Renal sympathetic nerve stimulation increases renin release at all arterial pressures, with a proportionately greater effect at pressures above 100 mm Hg.
The combined effects of low-frequency stimulation of the renal sympathetic nerves and reductions in renal arterial blood pressure on various hemodynamic parameters of the in situ kidney and on renal venous renin levels were determined in 17 dogs. Autoregulation of flow (measured using noncannulating electromagnetic probes) and glomerular filtration (measured using continuous extraction of 131 I-iothalamate) was followed before, during, and after nerve stimulation. Stimulation of isolated renal nerves (0.5 msec, 10-15 v, 0.1-3.0/sec) produced distinct changes in the release of renin with only minimal changes in the autoregulatory curves for glomerular filtration rate and renal plasma flow. Reducing arterial blood pressure from 150 to 50 mm Hg caused an increase in the release of renin from 4 to 35 ng/ml hour -1 . Stimulation of the renal nerves increased renin production at both pressures (from 4 to 10 ng/ml hour -1 at 150 mm Hg and from 35 to 50 ng/ml hour -1 at 50 mm Hg). In fact, renal nerve stimulation elicited increases in renin release at all pressures examined. In contrast, sodium excretion following nerve stimulation was depressed at comparable sodium loads in spite of minimal changes in renal hemodynamics. It appears that the effect of the renal sympathetic nerves on renin release is evident at all pressures; however, the sympathetic nerves are proportionately more important at pressures above 100 mm Hg and the renal artery pressure plays a greater role at pressures below 115-100 mm Hg.
Grange et al. (Sat,) studied this question.