KININ ACTIONS ON RENAL PAPILLARY BLOOD-FLOW AND SODIUM-EXCRETION

Infusion of bradykinin into the renal medullary interstitium (0.1 mug/ min, n=6) significantly increased renal papillary blood flow as measur ed by laser-Doppler flowmetry to 117+/-3% of control without altering cortical blood flow or blood pressure in anesthetized Munich-Wistar ra ts. In animals prepared for clearance studies, renal medullary bradyki nin infusion did not alter total renal blood flow, glomerular filtrati on rate, or renal interstitial hydrostatic pressure but increased urin e flow by 100%, sodium excretion by 111%, and fractional sodium excret ion by 107%. No changes occurred in mean arterial pressure or contrala teral kidney function during the interstitial bradykinin infusion. Blo ckade of endogenous kinin degradation by interstitial infusion of capt opril (1 mg/hr) significantly increased papillary blood flow by 21+/-5 % without altering cortical blood flow. Pretreatment with the nitric o xide inhibitor N(G)-nitro-L-arginine-methyl ester (2 mug/min, n=7) eli minated the increase in papillary blood flow associated with either br adykinin or captopril infusion. We conclude that renal medullary inter stitial infusion of bradykinin increases sodium and water excretion, w hich is associated with a selective increase in papillary blood How by a nitric oxide-dependent mechanism.