Modulation of renal blood flow and vascular tone by neuronal nitric oxide synthase-derived nitric oxide

Nitric oxide (NO) formed via neuronal nitric oxide synthase (nNOS) in renal vasculature and tissues and in the brain plays an important role in controlling renal hemodynamics, renal function, and systemic blood pressure. Activation of parasympathetic nitrergic nerves innervating renal vasculature contributes to vasodilatation in renal arteries and pre- and postglomerular arterioles, an increase in renal blood flow, and a decrease in vascular resistance. NO released from autonomic nitrergic nerves interferes with the release of norepinephrine from adrenergic nerve terminals or the amine actions on smooth muscle. The pre- or postjunctional mechanisms of NO actions participate in vasodilatation through a diminution of sympathetic vasoconstrictor influence. On the other hand, NO from neurons in the brain acts on the paraventricular nucleus of the hypothalamus and the rostral ventrolateral medulla and inhibits the central sympathetic nerve activity to the kidney, leading to renal vasodilatation and increased renal blood flow. The present article summarizes information concerning the renal blood flow and vascular tone through nNOS-derived NO produced in peripheral autonomic nerves and the brain. The nNOS-derived NO-cyclic GMP pathway would be an important target for the treatment of renal circulatory dysfunction and chronic kidney disease.