EFFECTS OF BRADYKININ AND PAPAVERINE ON RENAL AUTOREGULATION AND RENIN RELEASE IN THE ANESTHETIZED DOG

The present study on six anaesthetized dogs investigates the influences of two different vasodilators, bradykinin and papaverine, on the relationship between autoregulation of renal blood flow and glomerular filtration rate, sodium excretion and renin release. At control conditions renal blood flow and glomerular filtration rate was autoregulated to the same levels of renal arterial pressure, 55 +/- 3 and 58 +/- 3 mmHg, respectively. Renin release increased from 0.3 +/- 0.1 to 22 +/- 4-mu-g AI min-1, and sodium excretion decreased from 99 +/- 29 to 4.6 +/- 3.3-mu-mol min-1 when renal arterial pressure was reduced from 122 +/- 6 to 44 +/- 2 mmHg. Infusion of bradykinin (50 ng kg-1 min-1) increased renal blood flow by 50% at control blood pressure without changing glomerular filtration rate, and both renal blood flow and glomerular filtration rate autoregulated to the same pressure levels as during control. Sodium excretion increased threefold at control renal arterial pressure, but was unchanged at low renal arterial pressure. Bradykinin did not change renin release neither at control nor low renal arterial pressure. Papaverine infusion at a rate of 4 mg min-1 increased renal blood flow 50% without changing glomerular filtration rate. The lower pressure limits of renal blood flow and glomerular filtration rate autoregulation were increased to 94 +/- 6 and 93 +/- 6 mmHg, respectively. Sodium excretion increased sixfold at control renal arterial pressure and was still as high as the initial control values at low renal arterial pressure (97 +/- 27-mu-mol min-1) accompanied by only a small increase in renin release (1.4 +/- 0.3 to 6 +/- 2-mu-g AI min-1). We conclude that bradykinin does not influence autoregulatory pressure limits of renal blood flow and glomerular filtration rate nor the accompanying increase in renin release during reductions in renal arterial pressure. Papaverine on the other hand maintains high sodium chloride delivery to macula densa at low renal arterial pressure, suppressing renin release and impairing autoregulation through effects on the tubulo-glomerular feedback mechanism.