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University Institute Of Pharmacy, Pt. Ravishankar Shukla University, Raipur, Chhattisgarh- 492010
One of the most common chronic conditions in the world, hypertension significantly increases the risk of kidney, cardiovascular, and neurological problems. Despite the wide availability of synthetic antihypertensive medications, adverse effects, high prices, and poor adherence-particularly in areas with limited resources—often restrict long-term control. Due to these restrictions, there is now more interest in herbal remedies, many of which have long been essential components of traditional Chinese medicine, Ayurveda, and Unani. Vascular reconstruction, dysfunction of endothelial cells, oxidative stress, and abnormalities in signalling molecules like nitric oxide & hydrogen sulphide are some of the underlying causes of hypertension that are examined in this review. It also emphasizes how particular medicinal plants alter these pathways. Herbs with a variety of mechanisms of action, such as calcium channel inhibition, renin-angiotensin-aldosterone system regulation, nitric oxide enhancement, and antioxidant effects, such as Terminalia arjuna, Crataegus monogyna, Ginkgo biloba, Withania somnifera, Boerhaavia diffusa, Tribulus terrestris, Allium sativum, and Camellia sinensis, have antihypertensive activity. Their phytoconstituents, including withanolides, ginsenosides, allicin, and punarnavine, have demonstrated promise in reducing the risk of problems such as erectile dysfunction, nephropathy, atherosclerosis, stroke, and left ventricular hypertrophy. By combining pharmacological facts and molecular insights, this review emphasizes the importance of herbal drugs as long-term and effective adjuncts or alternatives for managing hypertension and its associated difficulties.
Hypertension, often known as high blood pressure, is a major public health issue around the world. By 2025, it is expected that more than 1.5 billion persons worldwide—or almost one in every three people aged 30 to 79—will have hypertension6. Despite advances in diagnosis and care, less than 20% of these people successfully control their blood pressure7. The issue is particularly grave in India, where around 24% of adult men and 21% of adults are affected1. Urban populations have prevalence rates that range from 25% to 30%, while rural areas have a bit lower estimate between 10% and 14%2. Even more concerning is that only about 37% of persons with hypertension obtain a diagnosis, 30% receive treatment, and less than 15% maintain ongoing blood pressure management3.
This growing burden, along with limited treatment accessibility and low long-term adherence, has rekindled interest in both traditional and alternative therapies, particularly those involving medicinal plants. Herbal therapies have been used for millennia in traditional practices such as Ayurveda, Traditional Chinese Medicine (TCM), and Unani, where botanicals are used to lower blood pressure, relieve stress, and improve 6vascular health. Recent pharmacological investigations have verified the blood pressure-lowering properties of several plants, include Rauwolfia serpentina, Allium sativum (garlic), and Hibiscus sabdariffa. These kinds of plants are high in bioactive substances-such as alkaloids, flavonoids, polyphenols, and saponins, which give antihypertensive benefits via mechanisms such ACE inhibition, vasodilation, antioxidant effects, and increased urine output4.
Given the prevalence of hypertension worldwide and the disadvantages of synthetic medications—such as side effects, increased costs, and the possibility of polypharmacy—herbal treatments for hypertension are gaining recognized as viable and sustainable supplementary solutions5,6,7. This review evaluates the existing evidence on herbal antihypertensive therapies, stressing their pharmacological effects, clinical effectiveness, safety profiles, and potential role in the holistic management of hypertension8.
Even though there are different therapeutic options to manage hypertension and cholesterol using regular drugs, blood pressure control remains unsatisfactory, particularly in low and middle-income countries9. This may be due to delays in intensifying treatment regimens like lifestyle changes and traditional medications, as well as a lack of awareness regarding the significance of adhering to prescribed treatments10,11. Worldwide, it has been discovered that 80% of individuals are open to the idea of using herbs for treating health issues, while the exclusive use of traditional herbal medicine among those with hypertension stood at 38.6%, with 47.5% using it in conjunction with antihypertensive medications12,13.
GRAPHICAL ABSTRACT
2.1 Search Strategy and Method for Identification of Studies
A literature search of published papers, periodicals, magazines, monographs, dissertations, and theses was part of this project. This time range was extended in certain cases because of incomplete information using the search terms "hypertensive," "hypotensive," "anti-hypertensive," and "blood pressure," along with their corresponding translations, the researchers identified medicinal plants that can alter blood pressure for this study through literature and other resources found in the Professor Eurico Back Library at UNESC. Research was also conducted using Medline, PubMed, Science Direct, academic Google, and Scientific Electronic Library Online to survey plant/drug interactions. The terms "antihypertensive drugs" (antihypertensives), "high blood pressure" (hypertension), and "drug interactions" were linked to the scientific names of plants that were found to alter blood pressure.The Gray search was conducted using Google Scholar as an extra platform, and substantial reference mining was done from the chosen papers. This was done to make sure that this systematic review did not omit any pertinent publications.
2.2 Pathophysiology of hypertension
The pathophysiological processes linked to the development of hypertension include increased vascular resistance, which is primarily identified by reduced vascular diameter due to increased arterial remodelling and vascular contraction14.Various elements play a role in the pathophysiology of hypertension (HTN), such as heightened activity of the renin-angiotensin-aldosterone system (RAAS), increased sympathetic nervous system stimulation, vasopressin effects, disruption of G protein-coupled receptor signalling, inflammatory responses, various functions of T-cells, and the range of vasoactive peptides released by other endothelial and smooth muscle cells15.
Molecular Pathogenesis of Hypertension
Hypertension is defined by abnormalities in the arteries throughout the vascular system, impacting major arteries like the aorta, smaller resistance vessels (150–400µm), and the microcirculation, which includes arterioles and capillaries. Heightened arterial reactivity (responsiveness and strength) results from a lack of proper regulation in the presence of endothelial nitric oxide synthase (e-NOS) and pro-oxidant enzymes, along with heightened basal and stimulated calcium levels resulting from excessive transmembrane calcium permeability via calcium channels, and/or the simultaneous occurrence of vascular smooth muscle cell (VSMC) hyperplasia and hypertrophy (vascular remodelling), can result in increased vasoconstriction. These pathological processes contribute to a greater ratio of the thickness of the vessel wall compared to the size of the arterial lumen16. The heightened ratio significantly contributes to the onset of hypertension.
Figure. 1 Pathophysiology of Hypertension
Vascular smooth muscle cells (VSMCs) play a role in the development of hypertension, and their growth leads to heightened peripheral resistance by reducing the diameter of arteries17. To gain an understanding of these complex changes, it is necessary to investigate the modifying variables that encourage or inhibit VSMC formation in the therapy of hypertension. Growth factors stimulate the cell to enter the cell cycle until the G1 phase, the first checkpoint. VSMC changes are a primary contributor to the development of hypertension. Normally, these cells are contractile and relaxed, which helps to regulate blood flow and vascular tone. However, in hypertension conditions, VSMCs become more active and lose their contractile properties. This shift, known as phenotypic flipping, allows them to proliferate, migrate, and produce more structural proteins, resulting in larger and more rigid blood vessels19.
Another signal, platelet-derived growth factor (PDGF), functions similarly by activating pathways that lead to enhanced VSMC proliferation and remodeling19. High blood pressure exerts mechanical pressures on VSMCs as well. Mechanosensitive molecules detect these stresses and activate pathways such as YAP/TAZ and RhoA/ROCK, promoting cell growth and shape alterations20. These modifications help to restrict and harden the arteries. Inflammation and oxidative stress exacerbate the situation. Increased amounts of reactive oxygen species (ROS) can activate pathways such as EGFR/AKT/ERK, resulting in additional cell growth. In addition, inflammatory molecules like as TLR4 and NF-KB are activated, promoting inflammation and driving VSMCs into an active, synthetic state21.
Figure. 2 Receptor-Mediated RAAS Pathways Contributing to Hypertension
A new study published in 2025 revealed the role of a protein known as ZFP36. This protein reduces the quantity of RGS2, which normally inhibits cell proliferation. When RGS2 is reduced, signals that induce contraction and cell growth become more powerful, exacerbating hypertension. In animal models, inhibiting ZFP36 in VSMCs helped lower blood pressure and enhance vascular shape22. Various signals cause this behaviour. One of the most significant is angiotensin II (Ang II), a chemical that causes high blood pressure. It activates the AT1R receptor on VSMCs, which stimulates intracellular pathways such as ERK and elevates calcium levels in the cells, boosting their development and migration23.
Several potential therapeutics are being investigated to prevent or treat VSMC overgrowth. One of these is Resolving D1, a molecule that reduces inflammation and inhibits damaging signalling pathways. Research indicates that it can inhibit Ang II-induced vascular remodelling and lower blood pressure in animals23.
Endothelial cells form a single layer that lines the interior surface of blood arteries and are critical for vascular function. These cells control processes like blood flow, vascular tone, inflammation, blood coagulation, and barrier permeability. In healthy settings, endothelial cells release chemicals like nitric oxide (NO), which helps relax blood arteries and prevent clot formation or severe inflammation24.
Endothelial cells frequently fail in the presence of hypertension and cardiovascular disease. This dysfunction can be caused by high levels of angiotensin II (Ang II), oxidative stress, and disrupted blood flow. Ang II not only increases blood pressure but also disturbs the protective role of endothelial cells by increasing the formation of reactive oxygen species (ROS), lowering nitric oxide bioavailability, and harming the inner lining of blood vessels25.
According to recent research, Ang II can cause endothelial cells to die through a process known as ferroptosis. This process is initiated by lipid peroxidation and involves receptors such as CD36, which absorb oxidized lipids and decrease the protective barrier created by these cells. As a result, the vascular wall is more susceptible to inflammation and injury26.
Oxidative stress is a primary cause of endothelial damage. When ROS levels rise due to mitochondrial malfunction or NADPH oxidase activation, they activate inflammatory pathways such as NF-KB, JAK/STAT, and MAPK. These signalling pathways promote the production of adhesion molecules like ICAM-1 and VCAM-1, which attract immune cells to the vascular wall and increase inflammation and remodeling27.
Figure. 3 Oxidative stress and role of NOS on blood vascular system
The following signalling molecules become essential to the pathophysiology of hypertension assuming a homeostatic imbalance28. Fortunately, various plant and herbal extracts, along with their individual metabolites, can influence signalling cascades related to the physiology of the cardiovascular system (refer to Section Herbs and Spices Most Commonly Used for Treatment of Hypertension, below). These herbs not only protect blood vessels but could also potentially reverse the changes associated with hypertension. This is especially true if changes in hypertensive patients are dealt with before they reach a decompensated state.
In a healthy state, pro-oxidant activity is counterbalanced by antioxidative agents. Nevertheless, when this balance is disrupted, the disorganized environment gives rise to pathological conditions like hypertension, atherosclerosis, and various other vascular complications29. ROS, such as superoxide anions (O•− 2) and hydroxyl ions (OH−), play a critical role in hypertension pathophysiology by causing oxidative stress30. Reactive oxygen species (ROS) are produced by nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and other enzymatic activities, particularly those associated with the electron transport chain in mitochondria31. ROS are also liable for the oxidation of low- density lipoprotein (LDL), which causes inflammation and increases VSMC proliferation. Inflammation and increased proliferation both play important roles in causing plaque formation, which may contribute to high blood pressure. Interestingly, in animals, blood pressure drops when ROS generation is reduced with antioxidant treatment32.
Nitric oxide (NO), a key chemical produced by endothelial cells, has a direct effect on vascular smooth muscle cells (VSMCs) and is required for the control of vascular tone, blood pressure, and pathologic remodelling. Under normal settings, No is mainly generated by endothelial nitric oxide synthesis (e-NOS) and spreads into vascular smooth muscle cells (VSMCs), which activates soluble guanylate cyclase (sGC). This activation increases the quantity of cyclic guanosine monophosphate (cGMP), which stimulates protein kinase G (PKG). PKG reduces cellular calcium levels, smooth muscle elasticity, and decreases VSMC proliferation and migration33.
Beyond the typical cGMP-dependent mechanisms, NO has cGMP-independent actions. One important method is S-nitrosation, in which NO covalently changes proteins such as RhoA and Raf-1, inhibiting their signaling capabilities. These proteins are implicated in the ERK/MAPK pathway, which typically promotes VSMC development and migration. Inhibiting this mechanism causes cell cycle arrest and decreased proliferation34.
Recent research has demonstrated that NO can control VSMC growth by modulating ubiquitin-proteasome pathways. Specifically, NO promotes the degradation of UbcH10, an E2 enzyme required for cell cycle progression. Downregulating UbcH10 causes arrest during the G1/S phase transition and lessens neointimal thickening after vascular damage35. Stimulating NADPH oxidase produces superoxide anion (O•− 2), which combines with NO to form peroxynitrite, a potent oxidant. This peroxynitrite then induces oxidative breakdown of the e-NOS cofactor tetrahydrobiopterin (BH4), yielding the inactive dihydrobiopterin (BH2). This produces more superoxide anion, which eventually lowers BH4 levels. As a result, a shift in balance from NO to superoxide production occurs, which is known as the uncoupling of NOS36.
In VSMCs and perhaps endothelial cells, cystathionine γ-lyase (CSE) converts L-cysteine to produce hydrogen sulphide (H2S)37. H2S has a vasorelaxant impact on VSMCs via increasing intracellular cGMP levels and activating ATP-dependent potassium channels37,38.
Hydrogen sulphide (H₂S) is recognized as an important gas transmitter for maintaining vascular health. In VSMCs, H₂S regulates physiological activities such relaxation, proliferation, migration, and oxidative stress resistance. The circulatory system manufactures it naturally through the enzyme cystathionine γ-lyase (CSE).H₂S relaxes vascular smooth muscle by activating ATP-sensitive potassium (K_ATP) channels, resulting in membrane hyperpolarization and decreased calcium influx. This reduces intracellular Ca²⁺ and promotes vasodilation39. H₂S prevents vascular calcification by activating the KEAP1-NRF2-NQO1 pathway, a key antioxidant mechanism. This reduces oxidative damage and inhibits signals that promote calcification in VSMCs40, H₂S's actions make it an attractive target for therapies to prevent vascular disorders such as hypertension, atherosclerosis, and restenosis.
Pathophysiology of Disease - Chronic high blood pressure increases afterload, which is the pressure the left ventricle must overcome to pump blood. As a result, myocardial cells expand, causing left ventricular hypertrophy (LVH) to maintain cardiac output. Nonetheless, this favorable hypertrophy can turn maladaptive over time, resulting in increased stiffness of the myocardium, fibrosis, poor relaxation (diastolic dysfunction), and eventually heart failure, whether with preserved or reduced ejection fraction41.
At the cellular level, elevated blood pressure activates hypertrophic signalling pathways such MAPKs and alters calcium control, resulting in contractile dysfunction and poor energy efficiency42.
Herbal Solutions and Mechanisms: -
Pathophysiology of Terminalia arjuna - The cardiotonic properties of Terminalia arjuna are well established. According to clinical research, taking 400 mg of Oxyjun® (standardized Arjuna extract) daily enhanced cardiac output by 6.3%, decreased tiredness by 22.5%, and improved left ventricular ejection fraction43. Mechanistically, its triterpenoids and flavonoids modulate intracellular calcium cycling, enhance myocardial contractility, and reduce oxidative stress-induced apoptosis in cardiac cells42.
The heart uses left ventricular hypertrophy to make up for elevated systemic vascular resistance in persistent hypertension. After maintaining cardiac output for a while, this adaptive mechanism turns maladaptive because of fibrosis, higher myocardial oxygen demand, and poorer diastolic relaxation. Eventually, these alterations lead to cardiac failure with a preserved or decreased ejection fraction43.
Key Pathways Involved include –
Phytoconstituents like Triterpenoids (arjunic acid, arjunolic acid), Flavonoids (arjunone, arjunolone), Glycosides, tannins, and minerals (especially CoQ10-like activity) constituents contribute to Arjuna’s antioxidant, anti-inflammatory, and cardiotonic properties. Terminalia arjuna modulates calcium ion channels and sarcoplasmic reticulum function, improving myocyte relaxation and contraction cycles, thus supporting both systolic and diastolic function. By downregulating caspase-3 and maintaining mitochondrial membrane potential, it prevents myocardial cell death. This is important for sustaining cardiac energy metabolism, particularly during ischemia stress44.
Pathophysiology of Crataegus monogyna - To maintain cardiac output, chronic hypertension raises afterload over time, which induces adaptive myocardial hypertrophy. This process eventually turns pathological because of:
These changes disrupt diastolic function, promote electrical remodelling, and increase the risk of systolic heart failure.
Pathophysiology of Disease - Chronic hypertension harms small blood vessels in the brain, leading to arteriosclerosis, lipohyalinosis, and the development of microaneurysms. This vascular condition increases the risk of haemorrhagic stroke because of blood vessel due to vessel blockage. Furthermore, hypertension weakens cerebral autoregulation, affects the integrity of the blood–brain barrier (BBB), elevates levels of inflammatory cytokines, and triggers neuronal apoptosis49,50.
Herbal Solutions and Mechanisms: -
Pathophysiology of Ginkgo biloba - GDLM enhances cerebral blood flow, inhibits platelet activating factor reducing thrombosis, protects endothelial cells, and promotes neuronal resistance to hypoxia through antioxidant mechanisms50. Ischemic stroke is caused by arterial obstruction, which leads to diminished cerebral blood flow, ATP depletion, glutamate-induced excitotoxicity, oxidative stress, and neuronal death. Hemorrhagic stroke occurs when blood vessels break, resulting in hematoma formation, oxidative damage, and inflammation. Ischemic stroke is caused by arterial obstruction, which leads to diminished cerebral blood flow, ATP depletion, glutamate-induced excitotoxicity, oxidative stress, and neuronal death. Hemorrhagic stroke occurs when blood vessels break, resulting in hematoma formation, oxidative damage, and inflammation.51 Ginkgo biloba, particularly its extract EGb 761, provides neuroprotection via antioxidant, anti-inflammatory, and vasodilating properties. Its flavonoids and terpenoids absorb free radicals, enhance mitochondrial activity, and increase nitric oxide-mediated vasodilation52. In hemorrhagic stroke, Ginkgo decreases edema and maintains the blood-brain barrier, limiting neuronal damage53.
Pathophysiology of Withania somnifera - In ischemic stroke, the cessation of cerebral blood flow causes oxidative stress, excitotoxicity, and activation of the inflammatory cascade. Ashwagandha mitigates these effects by reducing lipid peroxidation, inhibiting pro-inflammatory cytokines (e.g., TNF-α, IL-6), and enhancing endogenous antioxidant defences (e.g., superoxide dismutase, catalase)55.
In haemorrhagic stroke, where bleeding into brain tissue causes edema and neuronal injury, Ashwagandha reduces neuroinflammation and supports the integrity of the blood-brain barrier. Its ability to upregulate brain-derived neurotrophic factor (BDNF) promotes neurogenesis and neuronal recovery post-stroke56.
Pathophysiology of Disease - Renal arteriole constriction and thickening brought on by hypertension results in ischemia and damage to the glomeruli and tubules. Proteinuria, a decline in glomerular filtration rate (GFR), and a gradual loss of nephrons lead to chronic kidney disease (CKD)57.
Herbal Solutions and Mechanisms: -
Pathophysiology of Boerhaavia diffusa - Glomerular ischemia, arteriolar constriction, glomerulosclerosis, and progressive nephron loss because of persistently elevated intraglomerular pressure are the hallmarks of hypertensive nephropathy. The processes behind these changes include oxidative stress, fibrosis, inflammation, and activation of the renin-angiotensin-aldosterone system (RAAS)59.
Boerhaavia diffusa has nephroprotective properties by:
Pathophysiology of Tribulus terrestris - Consequently, the strain on the renal vasculature is reduced. By increasing the quantities of endogenous enzymes such as glutathione peroxidase and superoxide dismutase, it also strengthens antioxidant defences and combats oxidative damage. Additionally, it helps prevent immune-related tissue damage through its anti-inflammatory properties, which are mediated by the reduction of cytokines including TNF-α and IL-6. Crucially, new research indicates that T. terrestris may block pathways linked to fibrosis, including the TGF-β1/Smad axis, which is essential for the development of chronic renal scarring.62,63.
Pathophysiology of Disease - The endothelium deteriorates more quickly due to high blood pressure, which causes LDL to oxidize and plaque to form. Because of the increased arterial stiffness and clot formation, this increases the risk of peripheral artery disease and heart attacks. High blood pressure-induced endothelial damage leads to LDL oxidation and the formation of atherosclerotic plaques, increasing the risk of cardiovascular events42. Chronic arterial disease known as atherosclerosis is brought on by endothelial dysfunction, which is frequently brought on by smoking, diabetes, hypertension, or hyperlipidaemia64. Endothelial damage promotes the migration of low-density lipoprotein (LDL) into the intima, where it is oxidatively modified to become oxidized LDL (oxLDL), which sets off an inflammatory cascade65. When monocytes enter the artery wall, mature into macrophages, and generate foam cells, early fatty streaks are created. Fibrous plaque development is facilitated by the proliferation of smooth muscle cells and the deposition of extracellular matrix. TNF-α and IL-1β are examples of inflammatory mediators that increase matrix metalloproteinase activity, weakening plaques and raising the chance of rupture66. Reduced nitric oxide (NO) bioavailability, oxidative stress, and decreased vasodilation all contribute to vascular dysfunction, which in turn encourages thrombosis and vascular stiffness. Acute ischemia episodes and thrombus development are brought on by plaque rupture, which reveals thrombogenic material65.
Herbal Solutions and Mechanisms: -
Pathophysiology of Allium sativum - Plaques in atherosclerosis form because of endothelial dysfunction and lipid accumulation. Oxidized low-density lipoprotein (oxLDL) causes an inflammatory response that draws monocytes, which then change into foam cells, resulting in the creation of fatty streaks and the progression of plaques69. Garlic counteracts this process by blocking HMG-CoA reductase, lowering LDL cholesterol production, and decreasing LDL oxidation via antioxidant activity70. It increases nitric oxide (NO) generation, improves endothelial function and vasodilation, and lowers oxidative stress. Reducing cytokines like IL-6 and TNF-α can reduce plaque destabilization and vascular damage71,72. Allium sativum regulates lipid metabolism, oxidative stress, and vascular inflammation via various pathways, thereby addressing the fundamental pathophysiological causes of atherosclerosis and vascular dysfunction.
Pathophysiology of Camellia sinensis - Endothelial damage triggers atherosclerosis, which is then followed by the entry of LDL cholesterol into the intima, oxidative modification, and the recruitment of monocytes, which develop into foam cells and aid in the creation of plaque75. Vascular dysfunction is sustained by oxidative stress and inflammation, which lowers the bioavailability of nitric oxide. By scavenging reactive oxygen species, preventing LDL oxidation, and increasing endothelial nitric oxide synthase (eNOS) activity, green tea catechins—EGCG in particular—oppose these processes and improve vasodilation76. Additionally, catechins reduce vascular inflammation and stabilize plaques by downregulating inflammatory mediators such NF-κB, TNF-α, and interleukins77.
Pathophysiology of Disease - Hypertension-induced arterial stiffness and endothelial dysfunction impair blood flow to the penile tissue. Nitric oxide (NO) deficiency inhibits the smooth muscle relaxation necessary for erection. Reduced nitric oxide availability and increased vascular stiffness, which hinder blood flow to the erectile tissue, are the causes of erectile dysfunction42,78. Furthermore, cGMP is broken down more quickly by elevated phosphodiesterase type 5 (PDE5) activity, which restricts smooth muscle relaxation. Hormonal abnormalities like low testosterone can lower libido and erectile function, while chronic inflammation and vascular stiffness further impair penile hemodynamics79,80.
Herbal Solutions and Mechanisms: -
Pathophysiology of Panax ginseng - Endothelial dysfunction, reduced NO bioavailability, oxidative damage, hormonal dysregulation, and neurovascular impairment all contribute to poor penile hemodynamics83. Ginsenosides have been shown in animal studies to improve erectile function by influencing central dopaminergic pathways and increasing erectile responses. Ginsenosides also increase the activity of endothelial nitric oxide synthase (eNOS) and cyclic guanosine monophosphate (cGMP), which relaxes smooth muscles in the corpus cavernosum and improves penile blood flow. Additionally, ginsenosides prevent oxidative damage to the vascular endothelium, which preserves erectile capacity84.
Pathophysiology of Mucuna pruriens - Erectile function depends critically on nitric oxide (NO)-mediated vasodilation in penile tissue. M. pruriens enhances dopamine levels in the brain, activating the hypothalamic–pituitary–gonadal axis, leading to increased gonadotropins and testosterone release, which in turn supports NO synthesis and endothelial function. It also mitigates oxidative stress in the corpus cavernosum via antioxidant actions, protecting NO availability and penile tissue structure85,86.
|
S. N. |
Botanical Name (Common Name) |
Mechanism (s) of Action (Target receptor) |
Part Used |
Antihypertensive Phytoconstituents (Major Active) |
Chemical Structure |
References |
|
1. |
Terminalia arjuna (Arjuna) |
PPARα receptor activation
Ca²⁺-handling proteins
Endothelial nitric oxide (NO)
|
Stem bark |
Arjunolic acid, arjunic acid, arjunosides (glycosides), tannins, ellagic acid, gallic acid, flavonoids and oligomeric proanthocyanidins |
|
87, 88, 89
|
|
2. |
Crataegus monogyna (Hawthorn) |
Na⁺/K⁺-ATPase inhibition
Endothelial NO synthase (eNOS) activation
TGF-β1/Smad signaling inhibition |
Leaves/flowers, and berries |
Vitexin, Hyperoside, rutin, quercetin, procyanidins. |
|
90, 91, 92, 93, 94 |
|
3. |
Ginkgo biloba (Ginkgo) |
Endothelial NO synthase (eNOS) activation
Platelet-activating factor (PAF) receptor antagonism
NF-κB pathway inhibition |
Leaves |
Ginkgolide B Flavonoids (quercetin, kaempferol), ginkgolides, bilobalide |
|
95, 96, 97, 98 |
|
4. |
Withania somnifera (Ashwagandha) |
NMDA receptor modulation
Nrf2/ARE pathway activation NF-κB pathway inhibition |
Roots, leaves |
Withanolides Withaferin A, withanolide A sitoindosides |
|
99, 100, 101
|
|
5. |
Boerhavia diffusa (Punarnava) |
TGF-β1/Smad signaling inhibition
Renin–Angiotensin–Aldosterone System (RAAS) modulation
|
Roots, leaves |
Punarnavine, boeravinones Flavonoids alkaloids |
|
102, 103, 104, 105 |
|
6. |
Tribulus terrestris (Puncture Vine) |
TGF-β1/Smad signaling inhibition
Renin–Angiotensin–Aldosterone System (RAAS) modulation
Nrf2/ARE pathway activation |
Fruits, roots |
Protodioscin Saponins (dioscin), flavonoids Diosgenin, Polyphenols, alkaloids |
|
106, 107, 108, 109 |
|
7. |
Allium sativum (garlic) |
HMG-CoA reductase inhibition
NF-κB inhibition
eNOS activation → ↑ NO |
Bulb |
Allicin, S-allyl cysteine, ajoene, diallyl disulfide, flavonoids, diallyl trisulfide, Organosulfur compounds
|
|
110, 111, 112, 113 |
|
8. |
Camellia sinensis (Green Tea) |
HMG-CoA reductase inhibition
NF-κB pathway inhibition
eNOS activation → ↑ NO |
Leaves |
Epigallocatechin gallate (EGCG), catechins, theaflavins, flavonoids |
|
114, 115, 116, 117
|
|
9. |
Panax ginseng (Ginseng) |
eNOS activation → ↑ NO release
Nitrergic nerve signaling modulation
Nrf2/ARE pathway activation, ↓ ROS |
Root |
Ginsenosides Rg1 (Rb1, Rg3, Re, Rd), polysaccharides, flavonoids, Total ginsenosides |
|
118, 119, 120,
|
|
10. |
Mucuna pruriens (Velvet Bean) |
Dopamine D2 receptor activation
Hypothalamic–pituitary–gonadal (HPG) axis activation Nrf2/ARE pathway activation |
Seeds |
L-DOPA (Levodopa), alkaloids, flavonoids, saponins, phenolic compounds, antioxidants (quercetin, catechins)
|
|
121, 122, 123 |
Table No. 1 Herbal Approaches for Managing Hypertension with Their Mechanisms of Action.
Side effects are common with several antihypertensive medications used to treat hypertension. To treat it, scientific research suggests a variety of lifestyle changes as well as the application of appropriate medicinal plants.41 Certain herbs and spices contain secondary metabolites that have antihypertensive effects. Many herbal remedies help manage and lower hypertension by providing antioxidant, anti-inflammatory, and anti-apoptotic benefits, activating the e-NOS-NO signalling pathway, reducing endothelial permeability, and promoting angiogenesis.42
The list of medicinal plants that have been found to be useful in managing and treating hypertension is provided in Table 1.
|
S.N. |
Botanical Name |
Common Name |
Mechanism(s) of Action |
Part Used |
Antihypertensive Phytoconstituents (Major Active) |
Reference |
|
|
1. |
Allium sativum |
Garlic |
Vasodilation, ACE inhibition, antioxidant |
Bulb |
Allicin, S-allyl cysteine, diallyl disulfide |
124
|
|
|
2. |
Hibiscus sabdariffa |
Rosella |
Vasodilation via Anthocyanins, ACE inhibition, diuretic |
Calyx |
Anthocyanins (delphinidin-3-sambubioside), protocatechuic acid |
125
|
|
|
3. |
Crataegus oxyacanthine |
Hawthorn |
Ca2+ Channel blockage, Antioxidant, Vasodilation |
Berry |
Flavonoids (vitexin, rutin), oligomeric procyanidins |
126
|
|
|
4. |
Nigella sativa |
Black Cumin |
↓SNS stimulation, antioxidants, Ca2+ blockage |
Seed |
Thymoquinone, α-hederin, nigellidine |
127
|
|
|
5. |
Rauwolfia serpentina |
Sarpa Gandha |
Sympatholytic via reserpine, catecholamine depletion |
Root |
Reserpine, ajmaline, serpentine (indole alkaloids) |
128
|
|
|
6. |
Boerhavia diffusa |
Punarnava |
Diuretic, Ca²⁺ channel blockade, antioxidant |
Root |
Punarnavine, boeravinones (rotenoids) |
129
|
|
|
7. |
Moringa oleifera |
Drumstick |
Vasodilation, ACE inhibition, antioxidant |
Leaf |
Quercetin, chlorogenic acid, isothiocyanates |
130
|
|
|
8. |
Coptis chinensis |
Goldthread |
ACE inhibition, ↓Ang II, ↑e-NOS |
Rhizome |
Berberine, palmatine, coptisine |
131
|
|
|
9. |
Panax ginseng |
Ginseng |
↑NO production, vasorelaxation, anti-inflammatory |
Root |
Ginsenosides (Rb1, Rg1, Re) |
132
|
|
|
10. |
Apium graveolens |
Celery |
Ca²⁺ channel inhibition, diuretic |
Seed |
3-n-butylphthalide, apigenin, luteolin |
133
|
|
|
11. |
Salvia Miltiorrhiza |
Red sage |
K⁺ channel activation, ACE inhibition, antioxidant |
Root |
Tanshinones, salvianolic acid B, rosmarinic acid |
134
|
|
|
12. |
Peganum harmala |
Esfand |
NO modulation, vasodilation, monoamine oxidase inhibition |
Seed |
Harmine, harmaline (β-carboline alkaloids) |
135
|
|
|
13. |
Peperomia pellucida |
Shiny Bush |
ACE inhibition, antioxidant, diuretic |
Whole Plant |
Pellucidin A, quercetin, tannins |
136
|
|
|
14. |
Syzygium polyanthum |
Indonesian Bay-leaf |
Vasorelaxation via phenolics, NO-dependent pathways |
Leaf |
Phenolic acids, flavonoids (quercetin, rutin) |
137
|
|
|
15. |
Bidens Pilosa |
Blackjack |
Diuretic, NO pathway enhancement, Ca²⁺ channel inhibition |
Leaf |
Polyacetylenes, rutin, caffeic acid |
138
|
|
|
16. |
Andrographis paniculata |
Kalmegh |
ACE inhibition, Ca²⁺ & β-blockade, ↑NO |
Leaf/Aerial Parts |
Andrographolide, neoandrographolide |
139
|
|
|
17. |
Terminalia arjuna |
Arjuna |
Vasorelaxation, antioxidant, cardiotonic |
Bark |
Arjunolic acid, arjunosides, tannins |
140
|
|
|
18. |
Camellia sinensis |
Green Tea |
Antioxidant, vasorelaxant(polyphenols), ACE inhibition |
Leaf |
EGCG (epigallocatechin gallate), catechins, theaflavins |
141
|
|
|
19. |
Ocimum sanctum |
Holy basil |
Diuretic, antioxidant, vasodilatory flavonoids |
Leaf |
Eugenol, rosmarinic acid, ursolic acid |
142
|
|
|
20. |
Glycyrrhiza glabra |
Licorice |
Mineralocorticoid effect, though use limited due to ↑BP risk |
Root |
Glycyrrhizin, liquiritigenin (note: ↑BP risk) |
143 |
|
|
21. |
Cinnamomum zeylanicum |
Cinnamon |
Insulin sensitization, vasodilation, antioxidant |
Bark |
Cinnamaldehyde, procyanidins |
144
|
|
|
22. |
Withania Somnifera |
Ashwagandha |
↓Cortisol, antioxidant, ↑NO |
Root |
Withanolides, sitoindosides |
145
|
|
|
23. |
Valeriana officinalis |
Valerian |
CNS depressant, ↓SNS, sedative |
Root |
Valerenic acid, flavonoids |
146
|
|
|
24. |
Crocus sativus |
Saffron |
Ca²⁺ channel blocker, antioxidant |
Stigma |
Crocin, safranal, crocetin |
147
|
|
|
25. |
Phyllanthus amarus |
Bhumi amla |
Antioxidant, ACE inhibition |
Whole Plant |
Phyllanthin, hypophyllanthin, ellagic acid |
148
|
|
|
26. |
Justicia gendarussa |
Willow-leaved justicia |
Vasodilation, Ca²⁺ blockade |
Leaf |
Gendarusin A, flavonoids |
149
|
|
|
27. |
Tribulus terrestris |
Gokshura |
Diuretic, vasorelaxant saponins |
Fruit |
Protodioscin, saponins |
150
|
|
|
28. |
Eclipta alba |
Bhringraj |
Vasodilator, NO activation |
Whole plant |
Wedelolactone, ecliptine |
151
|
|
|
29. |
Vitex negundo |
Nirgundi |
Vasodilator, anti-inflammatory |
Leaf |
Flavonoids (luteolin, casticin), iridoids |
152
|
|
|
30. |
Barleria prionitis |
Vajradanti |
Diuretic, vasorelaxant |
Leaf |
Barlerin, iridoid glycosides |
153 |
|
|
31. |
Azadirachta indica |
Neem |
ACE inhibition, antioxidant, vasodilation |
Leaf |
Nimbin, nimbolide, quercetin |
154
|
|
|
32. |
Piper betle |
Betel leaf |
Vasorelaxation, calcium antagonism |
Leaf |
Hydroxychavicol, eugenol |
155
|
|
|
33. |
Leea indica |
Bandicoot berry |
Ca²⁺ channel blocker, anti-inflammatory |
Leaf |
Flavonoids, phenolic acids |
156
|
|
|
34. |
Centella asiatica |
Gotu Kola |
NO-mediated vasodilation, diuretic
|
Laef |
Asiaticoside, madecassoside |
157
|
|
|
35. |
Sida cordifolia |
Bala |
Adrenergic modulation, mild hypotensive |
Leaf |
Ephedrine, vasicinol (low doses hypotensive) |
158
|
|
|
36. |
Aegle marmelos |
Bael |
Antioxidant, vasodilation via polyphenols |
Leaf |
Marmelosin, aegeline, flavonoids |
159
|
|
|
37. |
Cissampelos pareira |
velvetleaf |
ACE inhibition, diuretic, antioxidant |
Root |
Cissampeline, hayatin (alkaloids) |
160
|
|
|
38. |
Solanum nigrum |
Black nightshade |
Diuretic, β-blocking potential |
Leaf |
Solamargine, solanine, flavonoids |
161
|
|
|
39. |
Cassia occidentalis |
Coffee senna |
Ca²⁺ channel blockade, diuretic |
Leaf |
Emodin, chrysophanol, anthraquinones |
162
|
|
|
40. |
Mentha piperita |
Peppermint |
Vasodilation, NO modulation |
Leaf |
Menthol, rosmarinic acid |
163
|
|
|
41. |
Tamarindus indica |
Tamarind |
ACE inhibition, diuretic, antioxidant |
Fruit pulp |
Procyanidins, tartaric acid, catechins |
164
|
|
|
42. |
Rosmarinus officinalis |
Rosemary |
Vasodilation, ACE inhibition, Ca²⁺ blockade |
Leaf |
Rosmarinic acid, carnosic acid, ursolic acid |
165
|
|
|
43. |
Mangifera indica |
Mango |
Polyphenol-mediated vasodilation |
Leaf/fruit |
Mangiferin, gallic acid, quercetin |
166
|
|
|
44. |
Curcuma longa |
Turmeric |
Antioxidant, NO modulation, anti-inflammatory |
Rhizome |
Curcumin, demethoxycurcumin |
167
|
|
|
45. |
Avena sativa |
Oats |
Diuretic, endothelial function improvement |
Grain |
Avenanthramides, β-glucan |
168
|
|
|
46 |
Olea europaea |
Olive leaf |
ACE inhibition, vasodilation, antioxidant |
Leaf |
Oleuropein, hydroxytyrosol, verbascoside |
169
|
|
|
47 |
Orthosiphon stamineus (syn. O. aristatus) |
Java tea |
Diuretic, RAAS modulation, antioxidant |
Aerial |
Rosmarinic acid, sinensetin, eupatorin |
170
|
|
|
48
|
Apocynum venetum |
Luobuma |
β-blocker–like, Ca²⁺ antagonism, anxiolytic (↓SNS) |
Leaf |
Flavonoids (hyperoside), quercetin glycosides |
170
|
|
|
49 |
Eucommia ulmoides |
Du-zhong |
ACE inhibition, NO↑, vasodilation |
Bark/Leaf |
Geniposidic acid, pinoresinol diglucoside |
171
|
|
|
50 |
Zingiber officinale |
Ginger |
Ca²⁺ channel blockade, ACE↓, vasodilation |
Rhizome |
6-Gingerol, shogaols |
170
|
|
|
51 |
Allium cepa |
Onion |
ACE↓, vasodilation, antioxidant |
Bulb |
Quercetin, sulfur compounds |
170
|
|
|
52 |
Elettaria cardamomum |
Green Cardamom |
|
Seed |
1,8-Cineole, terpinyl acetate, flavonoids |
172, 173 |
|
|
53 |
Beta vulgaris |
Beetroot |
Dietary nitrate → NO↑ vasodilation |
Root/juice |
Nitrate, betalains |
174, 175
|
|
|
54 |
Vitis vinifera (seed) |
Grape seed |
Endothelial function, ACE↓, antioxidant |
Seed Extract |
Procyanidins (OPCs), catechins |
176, 177
|
|
|
55 |
Linum usitatissimum |
Flaxseed |
NO↑, anti-inflammatory, RAAS modulation |
Seed |
α-Linolenic acid, lignans (SDG) |
178, 179
|
|
|
56 |
Theobroma cacao |
Cocoa |
NO↑ (endothelial), ACE↓ |
Bean |
Flavanols (epicatechin, catechin) |
180, 181
|
|
|
57 |
Punica granatum |
Pomegranate |
ACE↓, antioxidant, endothelial protection |
Juice/Peel |
Punicalagins, ellagic acid |
182, 183
|
|
|
58 |
Vaccinium myrtillus / spp. |
Bilberry/Blueberry |
NO↑, antioxidant |
Berry |
Anthocyanins (delphinidin/cyanidin glycosides) |
170
|
|
|
59 |
Glycine max |
Soybean |
Endothelial/estrogenic, RAAS modulation |
Seed |
Isoflavones (genistein, daidzein) |
170
|
|
|
60 |
Sesamum indicum |
Sesame |
Antioxidant, NO/endothelial effects |
Seed/Oil |
Sesamin, sesamolin, lignans |
170
|
|
|
61 |
Coriandrum sativum |
Coriander |
Ca²⁺ blockade, diuretic |
Seed/leaf |
Linalool, flavonoids |
170 |
|
|
62 |
Cuminum cyminum |
Cumin |
Vasodilation, antioxidant |
Seed |
Cuminaldehyde, terpenes |
170 |
|
|
63 |
Trigonella foenum-graecum |
Fenugreek |
Insulin sensitization, diuretic, NO↑ |
Seed |
Saponins (diosgenin), 4-hydroxyisoleucine |
170 |
|
|
64 |
Passiflora incarnata |
Passionflower |
Anxiolytic (↓SNS), vasodilation |
Aerial Parts |
Flavonoids (vitexin), harmala alkaloids (trace) |
170
|
|
|
65 |
Achillea millefolium |
Yarrow |
Vasodilation, diuretic |
Aerial Parts |
Flavonoids, azulenes |
170 |
|
|
66
|
Tilia cordata/platyphyllos |
Linden |
Vasodilation, mild diuretic, anxiolytic |
Flower/bract |
Flavonoids (tiliroside), volatile oils |
170 |
|
|
67 |
Leonurus cardiaca |
Motherwort |
Negative chronotropy, vasodilation |
Aerial parts |
Leonurine, stachydrine |
170
|
|
|
68 |
Urtica dioica |
Stinging nettle |
Diuretic, RAAS modulation |
Leaf/root |
Flavonoids, lignans, sterols |
170
|
|
|
69 |
Cynara scolymus |
Artichoke leaf |
Endothelial protection, diuretic |
Leaf |
Cynarin, chlorogenic acid |
170
|
|
|
70 |
Petroselinum crispum |
Parsley |
Diuretic, vasodilation |
Leaf/seed |
Apiol, myristicin, flavonoids |
170
|
|
|
71 |
Berberis vulgaris |
Barberry |
ACE↓, vasodilation |
Root/Bark |
Berberine, berbamine |
170 |
|
|
72 |
Berberis aristata |
Tree Turmeric |
ACE↓, vasodilation |
Root/Bark |
Berberine, palmatine |
170 |
|
|
73 |
Salvia officinalis |
Sage |
ACE↓, antioxidant |
Leaf |
Rosmarinic acid, carnosol |
170 |
|
|
74 |
Melissa officinalis |
Lemon Balm |
Anxiolytic, vasodilation |
Leaf |
Rosmarinic acid, flavonoids |
170 |
|
|
75 |
Morus alba |
White Mulberry |
ACE↓, vasodilation |
Leaf |
DNJ, quercetin, chlorogenic acid |
170 |
|
|
76 |
Nelumbo nucifera |
Lotus leaf |
Diuretic, lipids↓, vasodilation |
Leaf/embryo |
Nuciferine, flavonoids |
170
|
|
|
77 |
Stephania tetrandra |
Fangji |
Ca²⁺ channel blockade |
Root |
Tetrandrine, fangchinoline |
170
|
|
|
78 |
Panax notoginseng |
Notoginseng |
Endothelial NO↑, anti-inflammatory |
Root |
Notoginsenosides R1, Rg1, Rb1 |
184
|
|
|
79 |
Vernonia amygdalina |
Bitter Leaf |
Vasodilation, antioxidant |
leaf |
Vernodalin, flavonoids |
170 |
|
|
80 |
Uncaria tomentosa |
Cat’s claw (Peru) |
Vasodilation, anti-inflammatory |
Bark |
Oxindole alkaloids |
170
|
|
|
81 |
Hibiscus rosa-sinensis |
Chinese hibiscus |
Vasodilation, diuretic |
Flower/leaf |
Anthocyanins, flavonoids |
170 |
|
|
82 |
Houttuynia cordata |
Fish Mint |
Diuretic, endothelial effects |
Aerial parts |
Houttuynoside, quercitrin |
170
|
|
|
83 |
Bacopa monnieri |
Brahmi |
Anxiolytic (↓SNS), NO↑ |
Aerial parts |
Bacosides |
170
|
|
|
84 |
Tinospora cordifolia |
Guduchi |
Endothelial/anti-inflammatory |
Stem |
Tinosporaside, berberine-like alkaloids |
170
|
|
|
85 |
Persea americana |
Avocado |
Vasodilation, antioxidant |
Leaf/seed |
Flavonoids, phenolics |
170 |
|
|
86 |
Satureja khuzestanica/hortensis |
Savory |
ACE↓, antioxidant |
Aerial parts |
Carvacrol, thymol, rosmarinic acid |
170 |
|
|
87 |
Carica papaya |
Papaya |
Ca²⁺ blockade (preclinical), antioxidant |
Leaf/Seed |
Benzyl isothiocyanate, flavonoids |
170
|
|
|
88 |
Eleutherococcus senticosus (syn. Acanthopanax senticosus) |
Siberian ginseng |
Endothelial/NO modulation, adaptogenic (↓SNS) |
Root |
Eleutherosides |
170 |
|
|
89 |
Nardostachys jatamansi |
Spikenard |
Sedative (↓SNS), vasodilation |
Rhizome |
Jatamansone (valeranone) |
170
|
|
|
90 |
Cydonia oblonga |
Quince |
Vasodilation, antioxidant |
Leaf/ 95fruit |
Quercetin, chlorogenic acid |
170 |
|
|
91 |
Angelica sinensis |
Dong-quai |
Vasodilation, anti-platelet |
Root |
Ferulic acid, ligustilide |
184 |
|
|
92 |
Plantago major/asiatica |
Plantain |
Diuretic, anti-inflammatory |
Leaf/ Seed |
Aucubin, acteoside |
170 |
|
|
93 |
Alisma orientale |
Ze-xie |
Diuretic, RAAS modulation |
Rhizome |
Alisol A/B (triterpenes) |
184
|
|
|
94 |
Aspalathus linearis |
Rooibos |
ACE↓, antioxidant |
Leaf |
Aspalathin, nothofagin |
170 |
|
|
95 |
Scutellaria baicalensis |
Chinese skullcap |
ACE↓, vasodilation |
Root |
Baicalin, baicalein |
184 |
|
|
96 |
Portulaca oleracea |
Purslane |
NO↑, K⁺ channel activation, diuretic |
Aerial parts |
Omega-3s, flavonoids |
170
|
|
|
97 |
Ammi visnaga |
Khella |
Ca²⁺ channel blockade, vasodilation |
Fruit |
Khellin, visnagin |
170 |
|
|
98 |
Gynostemma pentaphyllum |
Jiaogulan |
AMPK/NO/endothelial effects |
Leaf |
Gypenosides (saponins) |
185
|
|
|
99 |
Nigella arvensis |
Wild black cumin |
Antioxidant, vasodilation, Ca²⁺ channel modulation |
Seed |
Thymoquinone derivatives, alkaloids |
186
|
|
|
100 |
Erythrina variegata |
Indian coral tree |
Ca²⁺ channel blockade, CNS depressant (↓SNS activity) |
Baak/ Leaf |
Isoflavonoids (erycristagallin), alkaloids |
187
|
Table No. 2 Other Effective medicinal plants on Hypertension:
Abbreviations:
ACE – Angiotensin-Converting Enzyme
Ang II – Angiotensin II
AT1R – Angiotensin II Type 1 Receptor
BBB – Blood–Brain Barrier
CKD – Chronic Kidney Disease
CNS – Central Nervous System
CoQ10 – Coenzyme Q10
CSE – Cystathionine γ-Lyase
ED – Erectile Dysfunction
EGCG – Epigallocatechin-3-Gallate
GDLM – Ginkgo Diterpene Lactone Meglumine
GFR – Glomerular Filtration Rate
HPG Axis – Hypothalamic–Pituitary–Gonadal Axis
H₂S – Hydrogen Sulphide
IL – Interleukin
LDL – Low-Density Lipoprotein
LVH – Left Ventricular Hypertrophy
MAPK – Mitogen-Activated Protein Kinase
NO – Nitric Oxide
NOS – Nitric Oxide Synthase
PAF – Platelet-Activating Factor
PDE5 – Phosphodiesterase Type 5
PDGF – Platelet-Derived Growth Factor
PKG – Protein Kinase G
RAAS – Renin–Angiotensin–Aldosterone System
ROS – Reactive Oxygen Species
SNS – Sympathetic Nervous System
TGF-β1 – Transforming Growth Factor Beta 1
TNF-α – Tumour Necrosis Factor Alpha
VSMC – Vascular Smooth Muscle Cell
CONCLUSION
One of the most difficult worldwide health problems is still hypertension, which has a major role in neurological, renal, and cardiovascular problems. While traditional antihypertensive medications continue to be the mainstay of treatment, their drawbacks in terms of adverse effects, cost, and patient compliance underscore the need for safer and more long-lasting substitutes. The renin-angiotensin-aldosterone system modulation, calcium channel blockade, nitric oxide enhancement, and antioxidant defence are some of the mechanisms by which herbal medicines, enhanced with a variety of phytoconstituents like flavonoids, alkaloids, saponins, and polyphenols, offer promising antihypertensive effects.
Terminalia arjuna, Crataegus monogyna, Ginkgo biloba, Withania somnifera, Allium sativum, and Camellia sinensis are important medicinal plants that show promise in managing hypertension and reducing its secondary complications, like cardiac hypertrophy, renal impairment, cerebrovascular injury, vascular dysfunction, and erectile disorders.
To fully realize the benefits of these herbal compounds, future research should focus on thorough clinical validation, standardized formulations, and long-term safety monitoring. By acting through a variety of pathways, their diverse phytoconstituents provide a comprehensive therapeutic strategy. By combining these ancient therapies with modern biomedical research, they can be used as supportive or complementary interventions.
REFERENCES
Bhoomika Swarnkar, Abhishek Nand, Lokprabha Hirwani, Harkesh Dadsena, Pushpendra Kumar, Chhavi Rahangdale, Yashika Israni, Helina Tandon, Umakant Sahu, Vishal Jain*, Narendra Kumar, A Review On The Role Of Herbal Medicine In Modulating Hypertension-Related Complications: Mechanistic Insights, Int. J. Sci. R. Tech., 2026, 3 (6), 457-490. https://doi.org/10.5281/zenodo.20567000
10.5281/zenodo.20567000