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Nephrol Dial Transplant (2000) 15: 448-451
© 2000 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Angiotensin II type 2 receptors in the kidney: evidence for endothelial-cell-mediated renal vasodilatation

Shuji Arima and Sadayoshi Ito

The Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan

Correspondence and offprint requests to: Shuji Arima MD, The Second Department of Internal Medicine, Tohoku University School of Medicine, 1–1 Seiryo-cho, Aoba-ku, Sendai, 980–8574, Japan.

Introduction

Angiotensin II (Ang II), the physiologically active component of the renin–angiotensin system, plays an important role in the regulation of the cardiovascular and renal systems. Based on their different pharmacological and biochemical properties, two distinct subtypes of Ang II receptor have been defined and designated as type 1 (AT1) and type 2 (AT2) receptors. While both AT1 and AT2 receptors belong to the seven-transmembrane, G-protein-coupled receptor family, the function and signalling mechanism of these receptor subtypes are quite different [1,2]. Extensive pharmacological evidence indicates that most of the well-characterized actions of Ang II (such as vasoconstriction, cell proliferation, and renal salt retention) are now generally considered to result from stimulation of AT1 receptors [1,2], whereas the functional role of AT2 receptor has not been well defined. However, recent studies suggest that the AT2 receptors exert the opposite effects of AT1 . . . [Full Text of this Article]

AT2-receptor-mediated action of Ang II in the kidney

Vasodilator action of AT2 receptors in renal microvessels

Renal AT2 receptors under pathological conditions, and concluding remarks

References


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