Contribution of renal sympathetic nerves to the urinary excretion of norepinephrine

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Abstract
Increased activity of the renal sympathetic nerves may result in increased urinary excretion of norepinephrine (NE). In the present study, unilateral electrical stimulation of the renal nerves of the rabbit was employed to test this hypothesis. Stimulation of the renal nerves to one kidney at 2 Hz (group I) produced no significant alteration of plasma NE concentration, glomerular filtration rate (GFR), or NE excretion by either kidney. Stimulation at 4 Hz (group II) caused statistically significant reductions of GFR and urine flow in experimental kidneys, but the urinary excretion of NE, per millilitre GFR, and the CNE/GFR ratios were significantly greater than prestimulation values. In another group of animals (group III), an inhibitor of cation-specific tubular transport, cyanine 863 (6 mg/kg, i.v.), significantly reduced the prestimulation urinary excretion of NE by 60–70% when compared with that of groups I or II. Stimulation of the renal nerves (4 Hz) in the animals of group III caused a significant reduction in GFR in the experimental kidney but did not alter the urinary excretion of NE or the CNE/GFR ratios. The results of these studies indicate that an increase in renal nerve activity causes an increase in the urinary excretion of NE, and that tubular secretion is responsible for the excretion of the neuronally released catecholamine.

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