The dopamine (DA) content of the canine renal cortex is greater than can be attributed to its presence in noradrenergic axons only. Most of the excess DA is in the outer part of the cortex. By fluorescence histochemistry numerous catecholamine‐containing axons are seen to be associated with renal cortical arteries and arterioles. The fluorescence is abolished following treatment of animals with 6‐hydroxydopamine or with reserpine, but is restored to some axons if reserpine is followed by systemic administration of 1‐DOPA. This procedure does not restore fluorescence to atrial noradrenergic axons after reserpine‐induced depletion. Pretreatment of animals with guanethidine abolishes axonal fluorescence and depletes tissue NA and DA from atrium, but in renal cortex the tissue DA level is little affected and some fluorescent axons remain. These results are discussed in the light of previous functional evidence for dopaminergic autonomic axons in the canine kidney.
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Bell et al. (1978) studied this question.
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