Homocysteine, or HCY, hyperhomocysteinemia, i.e., elevated plasma homocysteine levels, is an independent risk factor for peripheral vascular and cerebrovascular atherosclerosis, neurological and hypertensive heart disease. Hyperhomocysteinemia has been reported to mediate vascular injury in two ways: 1) by elevating blood pressure; and 2) by impairing the vasodilatory function of the endothelial diastolic factor NO. Hcy activates metalloproteinases, which induce collagen (protein) synthesis, leading to an imbalance in the elastin/collagen ratio, thereby destroying vascular elasticity. Endothelial tissue metabolites in the presence of hyperhomocysteinemia can alter the composition of vascular myocytes, leading to abnormal vascular function and hypertension. Hcy metabolism in the body produces H2S, which is a strong antioxidant and vasodilator. If Hcy levels are elevated in vivo, Hcy inactivates proteins, including endogenous metabolizing enzymes such as cystathione-gamma-synthase, through Hcylation. In this way, decreased H2S production due to hyperhomocysteinemia can cause hypertension and vascular disease. Angiotensin II is the major fragment of the renin-angiotensin system, and activation of the AT1 receptor leads to the production of reactive oxygen species clusters (ROS). Although studies have shown that AT1 receptors mediate the generation of ECM components, the regulation of AT1 receptors in the context of hyperhomocysteinemia and its corresponding outcome are not known. We demonstrated that Hcy in vascular endothelial cells induces AT1 receptor-induced MMP-9 and collagen synthesis. laggner et al. demonstrated that H2S inhibits ACE (angiotensin converting enzyme) activity in endothelial cells. Therefore, in the presence of hyperhomocysteinemia, decreased H2S production is likely to promote ACE activity, which leads to upregulation of angiotensin II followed by hypertension.