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The Antihypertensive Effects and Mechanisms of Huotan Jiedu Tongluo Decoction in Rats with H-Type Hypertension
Published on: May 17, 2024
Homocysteine and essential hypertension
Ramón Rodrigo1, Walter Passalacqua, Julia Araya
1Instituto de Ciencias Biomédicas, Programa de Farmacología Molecular y Clínica, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Insights
High homocysteine levels may contribute to essential hypertension by impairing blood vessel function. Supplementing with B vitamins and folic acid might help manage blood pressure, but more research is needed.
Area of Science:
- Cardiovascular Research
- Hypertension Pathogenesis
- Vascular Biology
Background:
- Essential hypertension mechanisms remain unclear, potentially involving vascular endothelial and smooth muscle cell dysfunction.
- Endothelial dysfunction can disrupt normal endothelium-dependent vasomotor regulation.
- Homocysteine is an emerging risk factor for cardiovascular disease.
Purpose of the Study:
- To review clinical and experimental data on homocysteine's role in essential hypertension pathogenesis.
- To explore the mechanisms by which homocysteine may influence blood pressure regulation.
Main Methods:
- Review of existing clinical and experimental data.
- Analysis of homocysteine's effects on vascular function, nitric oxide bioavailability, oxidative stress, and vascular wall properties.
Main Results:
- Elevated homocysteine diminishes nitric oxide-mediated vasodilation.
- High homocysteine levels increase oxidative stress and vascular smooth muscle cell proliferation.
- Homocysteine alters vascular wall elasticity, contributing to elevated blood pressure and endothelial oxidant injury.
Conclusions:
- Homocysteine is implicated in the pathogenesis of essential hypertension through vascular dysfunction.
- Vitamin B12, B6, and folic acid supplementation may offer an adjunctive therapy for hypertension.
- Further randomized controlled trials are required to confirm the efficacy and safety of vitamin therapy for hypertension.
Abstract:
The authors examine the available clinical and experimental data supporting the view that homocysteine, an alternative risk factor of cardiovascular disease, may play a role in the pathogenesis of essential hypertension. The mechanism of this disease has not been elucidated, but it may be related to impairment of vascular endothelial and smooth muscle cell function. Therefore, the occurrence of endothelial dysfunction could contribute to alterations of the endothelium-dependent vasomotor regulation. Elevated homocysteinemia diminishes the vasodilation by nitric oxide, increases oxidative stress, stimulates the proliferation of vascular smooth muscle cells, and alters the elastic properties of the vascular wall. Thus, homocysteine contributes to elevate the blood pressure. Also it is known that elevated plasma levels of homocysteine could lead to oxidant injury to the endothelium. The correction of elevated homocysteinemia by administration of vitamins B12 and B6 plus folic acid, could be a useful adjuvant therapy of hypertension. However, further controlled randomized trials are necessary to establish the efficacy and tolerability of these potentially therapeutic agents.
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