RENAL NERVES MODULATE THE SECRETION OF RENIN MEDIATED BY NON-NEURAL MECHANISMS

The authors investigated the role of efferent renal nerve activity in modulating the responses of renin secretion rate to suprarenal aortic constriction and to furosemide administration in female dogs. After the renal nerves had been sectioned, constriction of the suprarenal aorta decreased renal perfusion pressure (from 132 ± 5 to 51 ± 2 mm Hg) and renal blood flow (from 303 ± 21 to 149 ± 18 ml/min) and increased renin secretion rate (from 184 ± 49 to 2012 ± 499 ng/min). Stimulation of the renal nerves at very low frequency (0.25 Hz) had no significant effect on basal renin secretion rate, arterial pressure, renal blood flow, or urinary sodium excretion. Aortic constriction during this low level renal nerve stimulation resulted in a significant augmentation in the renin secretion rate response (from 358 ± 107 to 6988 ± 1600 ng/min), whereas the changes in renal blood flow and renal perfusion pressure were similar to those observed without nerve stimulation. Similarly, low level renal nerve stimulation (0.25 Hz) was found to augment the renin secretion rate response to the intravenous administration of furosemide (1.0 mg/kg bolus followed by 0.017 mg/kg per min). These data show that a very low level of renal nerve activity which by itself does not change arterial pressure, renal blood flow, urinary sodium excretion, or renin secretion rate, augments the release of renin in response to suprarenal aortic constriction or furosemide. Furthermore, these data provide direct evidence that the renal nerves modulate renin release mediated through nonneural mechanisms. Additional data are presented which show how these observations account for previously reported differences in renin secretion rate responses of innervated and denervated kidneys during aortic constriction and furosemide administration.