Role of L-arginine-nitric oxide pathway in hypertension

Abstract

The present study was designed to investigate the effect of L-arginine administration on patients with essential and secondary hypertension by measuring haemodynamic parameters, neuroendocrine hormones and indicators of nitric oxide (NO) release. Ten patients with essential hypertension and six with secondary hypertension (three with renovascular hypertension and three with primary aldosteronism) were enrolled in the study. L-Arginine was administered intravenously to the hypertensive patients. During L-arginine administration, blood pressure, heart rate, cardiac output and neuroendocrine hormones such as catecholamines, plasma renin activity and plasma aldosterone were measured. To examine whether L-arginine administration increases NO production, indicators of NO release in vivo such as plasma cyclic GMP, plasma citrulline and urinary excretion of nitrite and nitrate were measured simultaneously. During administration, mean arterial pressure decreased, heart rate increased, cardiac output increased and total peripheral resistance decreased. The indicators of NO release increased simultaneously during administration. Catecholamine and plasma renin activity, rather than increasing in response to L-arginine-induced hypotension as expected, showed no significant changes except in patients with renovascular hypertension. In all patients plasma aldosterone levels decreased significantly in response to L-arginine administration, regardless of basal plasma renin activity and aldosterone levels. These results suggest that exogenous L-arginine produces a vasodilatory effect by increasing NO production and that L-arginine, or released NO, modulates the release of neuroendocrine hormones in hypertensive subjects.