Abstract
See related article, pp 722–729 The renin-angiotensin system has a central role in the regulation of blood pressure and water balance. It is also a main target in the treatment of hypertension. Angiotensin II has 2 major receptors, the type 1 (AT1R) and the type 2 receptor (AT2R), both coupled to G proteins. Adverse vascular remodeling observed in cardiovascular diseases is attributed to AT1R, and a large number of relatively selective AT1R inhibitors are now used in patients. The effects of AT2R are usually presented as counteracting the effects exerted by AT1R. Consequently, some beneficial effects of the AT1R blockers (angiotensin receptor blocker) are commonly attributed to AT2R activation.1 Beneficial vascular effects of AT2R have now been proven by several studies. For example, AT2R stimulation reduces vascular RhoA/Rho kinase/myosin light chain phosphorylation in angiotensin II and AT1R antagonist valsartan-treated vascular smooth muscle cells in vitro, as well as in the aorta of spontaneously hypertensive rats chronically treated with candesartan.2 Altogether, previous studies suggest a role for vascular AT2R in blood pressure lowering during chronic AT1R blockade. Similarly, in hypertensive diabetic patients, chronic angiotensin receptor blocker treatment increases AT2R expression level and AT2R-dependent vasodilatation of mesenteric resistance arteries.3 Nevertheless, in the absence of AT1R inhibition, expression of AT2R varies a lot under physiological and pathophysiological conditions,4 and the relatively low selectivity of the antagonist PD123319 and the weak specificity of the agonist CGP42112 do not help fully understand the role …
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