Homocysteine and Essential 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.

The relationship between the levels of plasma total homocysteine and insulin resistance in uncomplicated mild-to-moderate primary hypertension

“…Recent studies indicating that tHcy lowering therapies reduce the BP support the possibility that the link between homocysteine and BP is causal. 6 To eliminate the possible overlapping effects of different factors on HT, we performed multiple linear regression analysis using either SBP or DBP as a dependent variable. This analysis suggested that tHcy levels were the most prominent factor for HT.…”

<b>Hyperhomocysteinemia</b>

“…11,16) Even mild hyperhomocysteinemia is a major risk factor for arterial vascular disease, independent of conventional risk factors, such as diabetes mellitus, cigarette smoking, or hyperlipidemia. [26][27][28] The mechanism may be related to impairment of vascular endothelial and smooth muscle cell function. It has been suggested that hyperhomocysteinemia diminishes vasodilatation by nitric oxide, increases oxidative stress, alters the elasticity of the vascular wall, and contributes to elevate the blood pressure.…”

“…It has been suggested that hyperhomocysteinemia diminishes vasodilatation by nitric oxide, increases oxidative stress, alters the elasticity of the vascular wall, and contributes to elevate the blood pressure. 28) Human studies have shown that high levels of homocysteine are associated with impaired endothelial-dependent vasodilatation in essential hypertension. It has been thought that an interaction between homocysteine and endothelium in hypertensive patients may promote thrombogenesis and atherogenesis, leading to adverse cardiovascular events.…”

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

“…It is possible that the ORs generated from hypercholesterolemia play a role in the genesis of post-PCI restenosis. Rodrigo et al (2003) reported that there was an association between essential hypertension and elevated levels of plasma homocysteine. The results of the present study show that 55% percent of the patients who developed restenosis had a history of hypertension.…”

“…As described by Prasad et al (1991) Stamler and Slivka (1996), endothelial relaxations are dependent on the bioavailability of endothelial NO synthetase (eNOS) to produce nitric oxide. Nitric oxide is critical for sustaining vascular homeostasis (Rodrigo et al 2003). The effect of preservation of the endothelium by NO is weakened by hyperhomocysteinemia (Prasad, 1999).…”