title: Stimulation of renal dopamine production during acute volume expansion requires the presence of intact vagi but not renal nerves.
abstract: We have previously reported that acute volume expansion (VE) with isotonic saline stimulates the production of renal dopamine (DA) which in turn contributes to the accompanying diuresis and natriuresis via activation of renal tubular DA-1 receptors. The purpose of the present study was to determine whether the presence of vagi and/or renal nerves is essential in order to activate the renal dopaminergic system during acute VE. Acute VE (6% body weight) with isotonic saline was performed in two groups of anesthetized rats, one of which served as sham control whereas the other was subjected to bilateral cervical vagotomy. The diuretic and natriuretic responses to acute VE did not differ between the sham control and vagotomized groups. However, urinary DA excretion (UDAV) was significantly increased in the sham control but not vagotomized group. Pretreatment with SCH 23390, a selective DA-1 receptor antagonist led to significant attenuation of the diuretic and natriuretic response to acute VE in the sham control but not vagotomized group. In another group of animals, the diuretic and natriuretic response to acute VE was studied in rats subjected to acute unilateral renal denervation. Basal UDAV was not significantly different between the denervated (DNX) kidney and the contralateral innervated (INX) kidney. Acute VE evoked diuresis and natriuresis in both kidneys, the response in the DNX kidney being significantly greater when compared to that in the INX kidney. UDAV increased significantly and to similar levels in both kidneys. Pretreatment with SCH 23390 led to attenuation of the diuretic and natriuretic response to acute VE in the DNX but not INX kidney. After DA-1 receptor blockade, the residual renal response to volume expansion in the DNX kidney did not differ significantly from that in the INX kidney. The results of this study suggest that 1) afferent vagal pathways appear to mediate the VE induced stimulation of renal DA production; 2) the increase in UDAV during acute VE occurs primarily through a mechanism which is independent of renal noradrenergic and putative dopaminergic nerves.
authors.affiliation: Department of Pharmacology, University of Houston, TX 77204-5515.
authors.forename: S S
authors.initials: SS
authors.lastname: Hegde
authors.forename: M F
authors.initials: MF
authors.lastname: Lokhandwala
mesh_terms: D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D001810:Blood Volume; D003714:Denervation; D004298:Dopamine / Q000096:biosynthesis*; D007552:Isotonic Solutions / Q000494:pharmacology; D007668:Kidney / Q000294:innervation / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000494:pharmacology; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*
chemical_list: D001552:Benzazepines; D007552:Isotonic Solutions; D012965:Sodium Chloride; D004298:Dopamine