Mode of nitric oxide action on the renal vasculature

Our study aimed to characterize the essential cellular pathways along which nitric oxide (NO) exerts its well-known vasodilatatory properties in the k idney. Using the isolated perfused rat kidney model we examined the roles o f potassium channels, cGMP-protein kinase activity and cAMP-phosphodiestera ses (PDE) in the effect of NO on renovascular resistance. We found that nei ther potassium channel activity nor G-kinase activity was essential for the vasodilatatory effect of NO. The effect of NO, however, was essentially mi micked by pharmacological inhibition of PDE-3, which is a cGMP-inhibitable PDE. As PDE-3 is strongly expressed in renal preglomerular vessels and NO s timulates cGMP formation in renal vessels, it appears likely that inhibitio n of cAMP degradation and consequently the cAMP pathway are crucially invol ved in mediating the effects of NO on renal vascular resistance.