Evidence for hemodynamic autoregulation of renin release.

To examine the relationship between renal arteriolar dilatation and renin release, arterial perfusion pressure in anesthetized dogs was lowered in steps within and below the range of autoregulation of renal blood flow. Renin release, determined by both bioassay and radioimmunoassay, averaged 2.7 ± 0.9 (SE) /u,g/min at control pressure and increased to 20.0 ±4 .1 (SE) /zg/min at the lowest autoregulating pressure, which averaged 66.4 ± 2.9 (SD) mm Hg. However, renin release then remained constant during further lowering of arterial perfusion pressure despite reductions in renal blood flow. This response was not significantly changed when sodium excretion was increased by intravenous infusion of mannitol. In another series of experiments, renin release was raised by reducing arterial perfusion pressure below the range of autoregulation, and control sodium excretion was reestablished by mannitol or saline infusion; renin release remained high. Therefore, renin release appears to be related to autoregulated dilatation of the renal arterioles, and it becomes maximal when the arterioles are completely dilated at the lowest pressure of autoregulation of renal blood flow. This mechanism is different from release mechanisms dependent on sodium delivery to the distal nephron.