Effects of cocaine and nomifensine on canine renal venous norepinephrine and dopamine content during electrical stimulation of the renal nerves.

Dopamine has been suggested to play a role in the regulation of renal blood flow following its neuronal release from within the kidney. Skepticism remains, however, as to whether a vascular dopaminergic innervation plays a physiologic role in renal blood flow regulation. Thus, to investigate this possibility, we examined whether electrical stimulation of the renal nerves evokes an overflow of dopamine into renal venous blood that could be augmented by cocaine or nomifensine, two inhibitors of presynaptic uptake. To verify uptake inhibition, the stimulation-induced overflow of norepinephrine (NE) was also examined. The increases in renal venous NE content observed during 0.5 and 2.0 Hz renal nerve stimulation were significantly increased by administration of cocaine (2.5 and 5.0 mg/kg) and nomifensine (1 mg/kg). Renal nerve stimulation (0.5 and 2.0 Hz) did not significantly increase free renal venous or total dopamine sulfate content before or following administration of either cocaine or nomifensine. Renal venous minus arterial dopamine content indicated that a neuronal release of dopamine into renal venous blood could not be clearly demonstrated in the canine kidney. These results do not support the existence of an active dopaminergic innervation of the renal vasculature involved in the regulation of renal blood flow.