Renal nerves modulate the secretion of renin mediated by nonneural mechanisms.

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Abstract
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 was studied. After the renal nerves were sectioned, constriction of the suprarenal aorta decreased renal perfusion pressure (from 132 .+-. 5 to 51 .+-. 2 mmHg) 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 Na excretion. Aortic constriction during this low level renal nerve stimulation caused a significant augmentation in the renin secretion rate response (from 358 .+-. 107 to 6988 .+-. 1600 ng/min); the change in renal blood flow and renal perfusion pressure were similar to those observed without nerve stimulation. Low level renal nerve stimulation (0.25 Hz) augmented the renin secretion rate response to the i.v. furosemide (1.0 mg/kg bolus followed by 0.017 mg/kg per min). A very low level of renal nerve activity, which by itself does not change arterial pressure, renal blood flow, urinary Na excretion or renin secretion rate, augments the release of renin in response to suprarenal aortic constriction or furosemide. Apparently the renal nerves modulate renin release mediated through nonneural mechanisms. Additional data show how the observations account for reported differences in renin secretion rate responses of innervated and denervated kidneys during aortic constriction and furosemide administration.