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(Hypertension. 2007;49:270.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Cross-Talk Between Angiotensin II Receptor Types 1 and 2

Potential Role in Vascular Remodeling in Humans

Ivonne Hernandez Schulman; Ming-Sheng Zhou; Leopoldo Raij

From the Nephrology and Hypertension Section, Veterans Affairs Medical Center and Division of Nephrology and Hypertension and Vascular Biology Institute, University of Miami Miller School of Medicine, Miami, Fla.

Correspondence to Leopoldo Raij, Nephrology-Hypertension Section, Veterans Affairs Medical Center, 1201 NW 16 St (Room A-1009), Miami, FL 33125. E-mail LRaij@med.miami.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Angiotensin (Ang) II exerts its important physiological functions through 2 distinct receptor subtypes, the type 1 (AT₁) and type 2 (AT₂) receptors.¹ The AT₁ receptor is expressed in diverse adult tissues, and its distribution is indicative of the fundamental role of Ang II on the regulation of cardiovascular and renal homeostasis. The predominant actions of Ang II, such as vasoconstriction, cellular proliferation and growth, renal sodium retention, and release of aldosterone, are linked to the activation of various signal-transduction pathways modulated by the AT₁ receptor. Although the AT₂ receptor is highly expressed in the fetus, its expression in adult tissues is low but increases in response to injury.^2–5

It has been demonstrated that AT₁ and AT₂ receptors have counterregulatory interactions in the cardiovascular system.² The AT₂ receptor has been shown to exert an inhibitory effect on the growth-promoting action of the AT₁ receptor.⁶ The cross-talk between AT₁ and AT₂ receptors has also been suggested to participate in the regulation of blood pressure. Ang II binding to the AT₁ receptor activates G protein-coupled phospholipase C and inositol-1,4,5-triphosphate, which increases intracellular Ca²⁺ levels resulting in vasoconstriction. On the other hand, Ang II binding to the AT₂ receptor activates a counterregulatory pathway to induce vasorelaxation via activation of the kinin/NO/cGMP system.^4,5 Indeed, it has been demonstrated that stimulation of the AT₂ receptor induces vasorelaxation in mesenteric, uterine, renal, coronary, and cerebral resistance vessels, as well as in large conduit vessels.^3–5 AT₂ receptor null mice manifest slightly higher blood pressures at baseline . . . [Full Text of this Article]

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