NITRIC-OXIDE, THE KIDNEY, AND HYPERTENSION

The acute administration of nitric oxide (NO) synthesis inhibitors red uces the renal capacity to excrete sodium under normal or volume expan ded conditions and increases renovascular resistances in the absence o f changes in systemic blood pressure (BP). This indicates a sensitivit y of renal vasculature higher than that of systemic vessels to NO synt hesis inhibition. Medullary circulation is the renovascular territory most dependent on NO availability. Thus, alterations in medullary bloo d now seems to account for the blunted pressure-natriuresis and sodium retention during acute NO synthesis inhibition. By contrast, during c hronic administration of L-arginine analogs, systemic BP rises and ove rrides initial sodium retention by a resetting of the pressure-natriur esis relationship. This BP increase appears to be dependent on an over expression of the actions of vasoconstrictor systems due to an imbalan ce created by the diminished NO production. Prolonged NO synthesis inh ibition not only elevates BP, but also produces renal vascular and par enchymal damage. Antihypertensive therapy impedes BP elevation and ame liorates kidney deterioration. Finally, there is evidence of the possi bility that a certain alteration in the L-arginine-NO pathway exists i n genetic models and in human essential hypertension. In conclusion, a ccording to the data contained in the literature, NO plays a significa nt role in the regulation of systemic and renal hemodynamics and excre tory function, and could participate in the development of hypertensio n. (C) 1997 American Journal of Hypertension, Ltd.