Kinin actions on renal papillary blood flow and sodium excretion

Infusion of bradykinin into the renal medullary interstitium (0.1 /rg/min, a=6) significantly increased renal papillary blood flow as measured by laser-Doppler flowmetry to I17±3% of control without altering cortical blood flow or blood pressure in anesthetized Munich-Wistar rats. In animals prepared for clearance studies, renal medullary bradykinin infusion did not alter total renal blood flow, glomerular filtration rate, or renal interstitial hydrostatic pressure but increased urine flow by 100%, sodium excretion by 111%, and fractional sodium excretion by 107%. No cbanges occurred in mean arterial pressure or contralateral kidney function during the interstitial bradykinin infUsion. Blockade of endogenous kinin degradation by interstitial infusion of captopril (1 mg/hr) significantly increased paplllaiy blood flow by 21±5% without altering cortical blood flow. Pretreatment with the nitric oxide inhibitor iV^c-nltro-L-arginine-methyl ester (µg/min, n=7) eliminated the increase in papillary blood flow associated with either bradykinin or captopril infUsion. We conclude that renal medullary interstitial infUsion of bradykinin increases sodium and water excretion, which is associated with a selective increase in papillary blood flow by a nitric oxide-dependent mechanism. (Hypertension 1993;21:961-965)