This review synthesizes evidence on the cardiovascular and renal effects of chronic nitric oxide inhibition, highlighting its role in hypertension and organ injury.
Mechanisms of NO inhibition in hypertension and organ injury remain preclinical; leaves open whether targeting these pathways improves patient outcomes.
T he discovery in 1987 that endothelium-derived nitric oxide (NO) mediates the vasodilatory effect of certain endothelium-dependent agonists 1,2 inaugurated the current huge field of NO biology. It is now recognized that NO plays essential roles in many diverse physiological processes and in some pathophysiologic events. Development of these concepts has been based largely on evidence obtained by limiting NO biosynthesis. This review is centered on the cardiovascular and particularly the renal functional and structural consequences of chronic pharmacologic NO inhibition by L-arginine analogues. We devoted special attention to the mechanisms of hypertension and organ injury that occur under these circumstances, while appreciating the inherent limitations surrounding interpretation of this data.
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Zatz et al. (1998) studied this question.
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