Release of Dopamine from the Kidney in vivo

Abstract

Renal sympathetic nerve activity influences several aspects of renal function, such as renal blood flow (RBF), sodium excretion and renin release (DiBona, 1982; Gottschalk et al., 1985). An abundant adrenergic innervation, the principal transmitter of which is NA, has been demonstrated in the afferent and efferent arterioles, the tubules and juxtaglomerular cells (Barajas and Mueller, 1973; Barajas et al., 1984). There is, however, also histochemical evidence favouring the existence of a subset of renal dopaminergic nerves located primarily in the cortical region of the canine kidney (Bell et al., 1978; Dinerstein et al., 1979; Bell and Muller 1982). These findings are of considerable interest, since NA and DA in several respects have opposite effects on renal function. Thus, NA evokes vasoconstriction and reduces sodium excretion (Gill and Casper, 1972), whereas DA evokes vasodilatation and increases sodium excretion (Meyer et al., 1967). In fact, a role for DA in the control of sodium balance has been invoked (McNay et al., 1965; Kuchel et al., 1978; Goldberg and Weder, 1980; Lee, 1982). However, relatively little is known about the control of neurogenic DA release in the kidney and even less about its functional role.