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(Hypertension. 2001;38:669.)
© 2001 American Heart Association, Inc.

Renin-Angiotensin System

Angiotensin II Type AT₂ Receptor mRNA Expression and Renal Vasodilatation Are Increased in Renal Failure

Rocío Bautista; Alicia Sánchez; José Hernández; Adebayo Oyekan; Bruno Escalante

From the Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del IPN (R.B., A.S., J.H., B.E.), México; and Center for Cardiovascular Diseases, College of Pharmacy and Health Sciences, Texas Southern University (A.O), Houston.

Correspondence to Bruno Escalante, MD, PhD, Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del IPN, México, D.F; 07360. E-mail bescalan{at}mail.cinvestav.mx

Abstract

Abstract—— Kidney failure is associated with changes in renal vascular responses to angiotensin (Ang) II. We characterized expression of Ang II receptors and the renal vasoconstrictor and vasodilator responses to Ang II in kidneys from sham-operated and kidney failure rats. In the isolated perfused kidney of sham-operated rats, Ang II (1, 2, 4, and 8 ng) increased perfusion pressure by 27±6, 41±10, 54±11, and 74±12 mm Hg, respectively. These responses were amplified by 62±10% (P<0.05) in kidney failure rats. Losartan (1 µmol/L), an angiotensin type 1 (AT₁) receptor blocker, abolished renal vasoconstriction induced by Ang II, unmasking a renal vasodilatation that was greater in kidney failure rats. CGP-42112 (1 µmol/L) or PD 123,319 (1 µmol/L), angiotensin type 2 (AT₂) receptor ligands, blunted Ang II-induced renal vasodilatation. In the renal tissue of kidney failure rats, there was a marked increase in expression of AT₁ and AT₂ mRNA receptor. Ang II-induced vasodilatation was blunted by eicosatetraynoic acid (1 µmol/L), the all-purpose inhibitor of arachidonic acid metabolism; clotrimazole (1 µmol/L), an inhibitor of epoxygenase-dependent arachidonic acid metabolism; or N-nitro-L-arginine methyl ester (L-NAME; 1 µmol/L), an inhibitor of NO synthesis. On stimulation with Ang II, 20-HETE was the predominant product released into the renal effluent of sham-operated rats, whereas epoxy-eicosatrienoic acids were the predominant products released into the effluent of kidney failure rats. These data suggest that during development of kidney failure, there is induction of the AT₂ receptors, which may account for increased Ang II-dependent vasodilatation through the predominant release of epoxyeicosatrienoic acids .

Key Words: receptors, angiotensin • cytochrome P450 • kidney failure • angiotensin II • arachidonic acid

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