Essential hypertension is a major risk factor for cardiovascular, cerebrovascular, and renal diseases. However, the underlying cause and pathologic mechanisms of essential hypertension are poorly understood. Vascular inflammation and endothelial dysfunction are implicated in the pathogenesis of hypertension based on associations with elevated expression of adhesion molecules and chemokines and dysfunctional nitric oxide synthase. Human cytomegalovirus (HCMV) has been implicated in several cardiovascular disorders, including atherosclerosis, coronary heart disease, and cardiac transplant arteriopathy. Recent studies have suggested that HCMV is associated with cardiovascular disorders through impaired endothelial nitric oxide synthase function and subsequent endothelial dysfunction, which manifest as impaired vasculature dilation in vivo. However, direct links between human cytomegalovirus infection and essential hypertension remain undefined. Based on current studies, we present a hypothesis that human cytomegalovirus is an opportunistic pathogen that causes essential hypertension by disrupting nitric oxide synthesis and immune defense and by activating inflammation and the renin-angiotensin system.
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