The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.
Interaction between perfusion pressure and sympathetic nerves in renin release by carotid baroreflex in conscious dogs.
