Published Online
on September 19, 2005

A more recent version of this article appeared on October 1, 2005

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Submitted on June 23, 2005
Revised on July 11, 2005

Rat Strain Effects of AT₁ Receptor Activation on D₁ Dopamine Receptors in Immortalized Renal Proximal Tubule Cells

Chunyu Zeng^*; Zheng Wang; Ulrich Hopfer; Laureano D. Asico; Gilbert M. Eisner; Robin A. Felder; and Pedro A. Jose

From the Department of Cardiology (C.Z.), Daping Hospital, Third Military Medical University, Chongqing, P.R. China; Departments of Pediatrics (C.Z., Z.W., L.D.A., G.M.E., P.A.J.) and Physiology and Biophysics (P.A.J.), and Internal Medicine (G.M.E.), Georgetown University Medical Center, Washington, DC; Department of Physiology and Biophysics (U.H.), Case Western Reserve School of Medicine, Cleveland, Ohio; Department of Pathology (R.A.F.), University of Virginia Health Sciences Center, Charlottesville, Va.

^* To whom correspondence should be addressed. E-mail: cyzeng1{at}hotmail.com.

Abstract--The dopaminergic and renin-angiotensin systems regulate blood pressure, in part, by affecting sodium transport in renal proximal tubules (RPTs). We have reported that activation of a D₁-like receptor decreases AT₁ receptor expression in the mouse kidney and in immortalized RPT cells from Wistar-Kyoto (WKY) rats. The current studies were designed to test the hypothesis that activation of the AT₁ receptor can also regulate the D₁ receptor in RPT cells, and this regulation is aberrant in spontaneously hypertensive rats (SHRs). Long-term (24 hours) stimulation of RPT cells with angiotensin II, via AT₁ receptors increased total cellular D₁ receptor protein in a time- and concentration-dependent manner in WKY but not in SHR cells. Short-term stimulation (15 minutes) with angiotensin II did not affect total cellular D₁ receptor protein in either rat strain. However, in the short-term experiments, angiotensin II decreased cell surface membrane D₁ receptor protein in WKY but not in SHR cells. D₁ and AT₁ receptors colocalized (confocal microscopy) and their coimmunoprecipitation was greater in WKY than in SHRs. However, AT₁/D₁ receptor coimmunoprecipitation was decreased by angiotensin II (10^-8M/24 hours) to a similar extent in WKY (-22±8%) and SHRs (-22±12%). In summary, these studies show that AT₁ and D₁ receptors interact differently in RPT cells from WKY and SHRs. It is possible that an angiotensin II-mediated increase in D₁ receptors and dissociation of AT₁ from D₁ receptors serve to counter regulate the long-term action of angiotensin II in WKY rats; different effects are seen in SHRs.

Key words: dopamine • kidney • receptors, angiotensin II • rats, spontaneously hypertensive

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