Renal venous outflow and urinary excretion of norepinephrine, epinephrine, and dopamine during graded renal nerve stimulation.

Abstract

The effect of renal nerve stimulation (RNS) on renal venous outflow and urinary excretion of endogenous norepinephrine, epinephrine, and dopamine was examined in anesthetized dogs. In the unstimulated denervated kidney, there was a negative venoarterial concentration difference for all catecholamines. Low-level RNS (LLRNS) caused small changes in renal hemodynamics and renal venous outflow of dopamine and increased norepinephrine outflow by 3.22 +/- 0.95 pmol X min-1 X g-1 (n = 5, P less than 0.05). High-level RNS (HLRNS) reduced renal blood flow by 50% and increased renal venous outflow of norepinephrine and dopamine by 9.58 +/- 0.67 and 0.46 +/- 0.05 pmol X min-1 X g-1, respectively (n = 27, P less than 0.01 for both). Renal uptake of epinephrine was unchanged by HLRNS. The urinary excretion of norepinephrine but not dopamine was increased to a similar degree following RNS at both levels. HLRNS caused a similar increase of the urinary norepinephrine excretion from the contralateral denervated and unstimulated kidney. This could be explained by the increase in arterial norepinephrine (from 0.74 +/- 0.08 to 1.20 +/- 0.14 nM, P less than 0.01) caused by HLRNS as shown by experiments with intravenous infusions of norepinephrine. The alpha-adrenoceptor antagonist phenoxybenzamine counteracted the hemodynamic response to HLRNS and enhanced the renal venous outflow and urinary excretion of norepinephrine and dopamine. Our results indicate that renal nerves release dopamine as well as norepinephrine and that urinary catecholamine excretion is a poor indicator of intrarenal catecholamine release.