Increased release of norepinephrine and dopamine from canine kidney during bilateral carotid occlusion.

Abstract

The renal overflow of norepinephrine (NE) and dopamine (DA) to plasma from the innervated kidney was studied at rest and during sympathetic nervous system activation by bilateral carotid artery occlusion (BCO) in vagotomized dogs under barbiturate or barbiturate/nitrous oxide anesthesia. BCO elevated arterial pressure and the arterial plasma concentrations of NE, DA, and epinephrine (Epi). Renal vascular resistance (renal arterial pressure kept constant) increased by 15 +/- 7% (P less than 0.05) and the net renal venous outflows (renal venoarterial concentration difference X renal plasma flow) of NE and DA were enhanced (P less than 0.05). To obtain more correct estimates of the renal contribution to the renal venous catecholamine outflow, we corrected for the renal extraction of arterial catecholamines, assessed as the extractions of [3H]NE, [3H]DA, or endogenous Epi. The [3H]NE corrected renal NE overflow to plasma increased from 144 +/- 40 to 243 +/- 64 pmol X min-1 (P less than 0.05) during BCO, which, when compared with a previous study of the [3H]NE corrected renal NE overflow to plasma evoked by electrical renal nerve stimulation, "corresponds" to a 40% increase in nerve impulse frequency from approximately 0.6 Hz. If the renal catecholamine extraction was not taken into account the effect of BCO was underestimated. The renal DA overflow to plasma was about one-fifth of the NE overflow both at rest and during BCO, indicating that there was no preferential activation of noradrenergic or putative dopaminergic nerves by BCO.