Activation of angiotensin II type 1 receptors increases D dopamine receptor expression in rat renal proximal tubule cells.

Both the dopaminergic and renin-angiotensin systems play important roles in the regulation of blood pressure. Our previous study showed that the stimulation of dopaminergic D receptors reduced angiotensin II type 1 (AT) receptor expression in renal proximal tubule (RPT) cells. In this study, we tested whether AT receptors, in return, would regulate D receptor expression and function in RPT cells. Expression of the D receptor from Wistar-Kyoto (WKY) or spontaneously hypertensive rats (SHRs) RPT cells and renal cortex tissues were determined by western blot, and Na-K ATPase activity was determined using an enzyme assay. Urine volume and urine sodium of WKY rats and SHRs treated with or without D receptor stimulation were measured. Thus, activation of AT receptors with angiotensin II (Ang II) increased D receptor protein expression in RPT cells, and this increase was blocked by nicardipine, a calcium influx blocker. The D receptor agonist PD168077 inhibited Na-K ATPase activity in WKY RPT cells but not in SHR RPT cells. Ang II pre-treatment promoted D receptor-mediated inhibition of Na-K ATPase in RPT cells in WKY rats but not in SHRs. Meanwhile, Ang II pre-treatment augmented the natriuretic effect of PD168077 in WKY rats but not in SHRs. In conclusion, AT stimulation can regulate the expression and natriuretic function of dopaminergic D receptors in RPT cells and might be involved in the pathogenesis of essential hypertension.