title: Regulation of sodium transport by endogenous dopamine production in proximal tubular and OK cells.
abstract: Inhibition of AADC for several hours increases the activity and mass of NaKATPase in proximal tubular basolateral membranes and reduces phosphate (P1) and citrate excretion, but has only a small effect on Na excretion. The reduction in citrate excretion is consistent with the observed increase in brush border Na+/H+ exchange. Thus, in Na replete rats, endogenous D inhibits Na entry into proximal tubular cells, through cotransport with Pi and exchange with H+, and inhibits exit through the Na pump. Tonic D inhibition of NaKATPase and Na+/H+ antiporter activity is not found in the SH rats' kidneys, which have defective linkage of proximal tubular D receptors to adenylate cyclase. The inhibitory action of endogenous D on Pi reabsorption is retained in SHR kidneys. This suggests that different signaling systems are responsible for the effects of D on NaPi transport and Na+/H+ exchange. In OK cells D inhibits NaPi cotransport (Ki 0.2 microM). The D effect is not blocked by cAMP, adenylate cyclase, PKA or PKC inhibitors. Thus it appears that D regulates NaPi transport by a non-cAMP, non-PKC mechanism and is a homeostatic regulator of phosphate reabsorption by SHR.
authors.affiliation: Department of Clinical Biochemistry, University of Toronto, Ontario, Canada.
authors.forename: A D
authors.initials: AD
authors.lastname: Baines
authors.forename: R
authors.initials: R
authors.lastname: Drangova
mesh_terms: D000818:Animals; D001692:Biological Transport; D002460:Cell Line; D004298:Dopamine / Q000502:physiology*; D006973:Hypertension / Q000378:metabolism / Q000473:pathology; D007687:Kidney Tubules, Proximal / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000378:metabolism
chemical_list: D015222:Sodium Channels; D012964:Sodium; D004298:Dopamine