Angiotensin II regulation of renal dopamine uptake and Na+, K+-ATPase activity

CHOI MR; MEDICI C; GIRONACCI MM; CORREA AH; FERNÁNDEZ BE

NEPHRON PHYSIOLOGY

KARGER

Lugar: Basel; Año: 2009 vol. 111 p. 53 - 58

1660-2137

Backgroung/Aims: Angiotensin II (ANG II) decreases dopamine (DA) uptake in renal cortex activating AT1 receptors. We investigated the signaling pathways that mediate this action and the incidence of DA-ANG II interaction on renal Na+, K+-ATPase activity. Methods: ANG II effects on [3H]-DA uptake and Na+, K+-ATPase were measured in samples from outer renal cortex of Sprague-Dawley rats. Results: The inhibition of phospholipase C (PLC) pathway blunted ANG II inhibitory effects on [3H]-DA uptake, since U-73 122, 2-APB, TMB-8, Chelerythrine and KN-93 (PLC, IP3-dependent Ca2+ release channels, IP3 receptors, PKC and CaM kinase II inhibitors, respectively), each one blocked ANG II effects. Inhibition of adenylate cyclase pathway did not modify ANG II inhibitory effects on DA uptake. ANG II effects on [3H]-DA uptake were able to modify Na+, K+-ATPase activity in carbidopa treated rats. Exogenous DA decreased while ANG II increased the enzyme activity. Neither the addition of DA together with ANG II, nor the extraneuronal DA uptake blocker, hydrocortisone, altered ANG II stimulatory effects on Na+, K+-ATPase activity, but hydrocortisone blocked the inhibitory effects of exogenous DA. Conclusion: Stimulation of renal AT1 receptors by ANG II signals through PLC pathway to inhibit extraneuronal DA uptake. DA and ANG II act through a common pathway involving reversible renal tubular Na+, K+-ATPase deactivation and activation, respectively. In addition, ANG II by itself is able to stimulate renal Na+, K+-ATPase activity.