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(Hypertension. 2005;45:115.)
© 2005 American Heart Association, Inc.

Scientific Contributions

Selective Silencing of Angiotensin Receptor Subtype 1a (AT_1aR) by RNA Interference

Jorge Vázquez; María F. Correa de Adjounian; Colin Sumners; Aaron González; Carlos Diez-Freire; Mohan K. Raizada

From the Department of Physiology and Functional Genomics (J.V., C.S., A.G., C.D.-F., M.K.R.), University of Florida College of Medicine and McKnight Brain Institute, Gainesville, Fla; and the Instituto de Medicina Experimental (M.F.C.d.A.), Universidad Central de Venezuela, Caracas, Venezuela.

Correspondence to Mohan K. Raizada, PhD, Professor, Department of Physiology and Functional Genomics, College of Medicine, University of Florida, McKnight Brain Institute, Gainesville, FL 32610. E-mail mraizada{at}phys.med.ufl.edu

Angiotensin II exerts its physiological effects by activating multiple subtypes of its receptor such as AT_1a-, AT_1b-, and AT₂-receptors. Because of a high degree of similarity among these G-protein–coupled receptors, it has been difficult to assign diverse physiological actions of angiotensin II through these receptor subtypes. We have developed small interfering RNAs to selectively inhibit the expression of the AT_1a receptor (AT_1aR) subtype. A dsRNA, AT₁ 47, was found to be highly selective and efficient in reducing the levels of AT_1aR subtype. Transfection of AT_1aR-expressing CHO cells with dsRNA AT₁ 47 resulted in an 80% decrease in the AT_1aR expression. In contrast, dsRNA AT₁ 47 showed no significant effects on both AT_1bR and AT₂R subtypes. Thus, AT₁ 47 provides us with a powerful tool to selectively silence this subtype of receptor to investigate its role in cardiovascular physiology.

Key Words: receptors, angiotensin II • gene therapy • receptors, angiotensin

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