Mediatory role of endothelium-derived nitric oxide in renal vasodilatory and excretory effects of bradykinin.

Intrarenal infusions of 5 ng/kg/min bradykinin (BK) in 5 mg/kg intravenous bolus meclofenamate-treated anesthetized dogs significantly increased renal blood flow, diuresis, natriuresis, and kaliuresis. All these effects were abolished by the simultaneous intrarenal infusion of a competitive inhibitor of nitric oxide synthesis, NG-monomethyl-L-arginine (LNMMA). Furthermore, the intrarenal infusion of this inhibitor alone also produced a significant decrease in basal renal blood flow. The administration of L-arginine, a precursor of nitric oxide, prevented the inhibitory effect of LNMMA on the renal vasodilatory and excretory response to BK. Glomerular filtration rate and mean arterial pressure did not change throughout the experiment. It is concluded that the renal vasodilatory and excretory responses to intrarenal BK in meclofenamate-treated dogs are largely dependent on endothelium-derived nitric oxide.