Differences in cardiovascular morbidity and mortality from hypertension may result from variations in endothelial nitric oxide function.
Hypothesis-generating for endothelial nitric oxide in hypertension outcomes; does not support clinical interventions yet.
Hypertension is a common disorder. The morbidity and mortality attributed to hypertension are not uniform across patient populations. In certain individuals hypertension is accompanied by adaptive changes that involve the kidney, heart and blood vessels. Nitric oxide is a ubiquitous molecule that is upregulated by endothelial cells in response to shear stress and cyclic strain associated with hypertension. Experimental studies in animals have suggested that vascular upregulation of nitric oxide is an adaptive mechanism to increased blood pressure that may help in the prevention of end-organ damage. If these studies are applicable to humans, differences in cardiovascular morbidity and mortality from hypertension may result, at least in part, from the variation in endothelial function in response to hypertension.
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Ishani et al. (1999) studied this question.
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