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(Hypertension. 1998;32:1049-1053.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Dopamine D₁ Receptor and Protein Kinase C Isoforms in Spontaneously Hypertensive Rats

Lynne P. Yao; Xiao Xi Li; Pei-Ying Yu; Jing Xu; Laureano D. Asico; Pedro A. Jose

From the Walter Reed Army Medical Centers (L.P.Y.) and Georgetown University Medical Center, Washington, DC.

Correspondence to Dr Pedro A. Jose, Georgetown University Medical Center 2-PHC, 3800 Reservoir Rd NW, Washington, DC 20007. E-mail josep{at}gunet.georgetown.edu

Abstract—Dopamine, via D₁-like receptors, stimulates the activity of both protein kinase A (PKA) and protein kinase C (PKC), which results in inhibition of renal sodium transport. Since D₁-like receptors differentially regulate sodium transport in normotensive and hypertensive rats, they may also differentially regulate PKC expression in these rat strains. Thus, 2 different D₁-like agonists (fenoldopam or SKF 38393) were infused into the renal artery of anesthetized normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (n=5 to 6/drug/strain). Ten or 60 minutes after starting the D₁-like agonist infusion, both the infused kidney and the noninfused kidney that served as control were prepared for analysis. The D₁-like agonists produced a greater diuresis and natriuresis and inhibited Na⁺,K⁺-ATPase activity in proximal tubule (PT) and medullary thick ascending limb (mTAL) to a greater extent in WKY (20±1%) than in SHR (7±1%, P<0.001). D₁-like agonists had no effect on PKC- or PKC- expression in either membrane or cytosol but increased PKC- expression in PT in both WKY and SHR at 10 minutes but not at 60 minutes. However, membranous PKC- expression in PT and mTAL decreased in WKY but increased in SHR with either 10 or 60 minutes of D₁-like agonist infusion. D₁-like agonists also decreased membranous PKC- expression in PT and mTAL in WKY but increased it in PT but not in mTAL in SHR. We conclude that there is differential regulation of PKC isoform expression by D₁-like agonists that inhibits membranous PKC- and PKC- in WKY but stimulates them in SHR; this effect in SHR is similar to the stimulatory effect of norepinephrine and angiotensin II and may be a mechanism for their differential effects on sodium transport.

Key Words: receptors, dopamine • kidney tubules, proximal • renal medulla • protein kinase C

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