Abstract
Angiotensin II (Ang II) activates at least two high-affinity plasma-membrane receptors, the Ang-II type-1 (AT1) and type-2 (AT2) receptors. AT1 receptor (AT1R) subtype is expressed ubiquitously and is the one thought to be involved in all the well-known vascular biological effects of Ang II. The AT2 receptor (AT2R) subtype, on the other hand, is present in endothelial and smooth muscle cells in many vessel types and has a distribution that is not homogenous and varies with age, species, vessel type and pathophysiological state. Although the physiological role performed by AT2R has long remained an enigma, a role for this subtype in control of blood pressure has been proposed. It is suggested that AT2R, following their activation by Ang II, produce vasodilation in part through an action mediated by endothelium-derived nitric oxide. Here, we introduce our recent findings that in the smooth muscle of resistance arteries, AT1R (when activated by Ang II) attenuates an endothelium-dependent relaxation by inhibiting the action of cGMP. While, an activation of AT2R enhances the endothelium-dependent, nitric oxide-mediated relaxation, in part due to an enhancement of the cGMP-action. Thus, importance of the function of AT2R is suggested on Ang II-induced regulation of nitric oxide-mediated relaxation in resistance arteries. [Jpn J Physiol 55 Suppl:S52 (2005)]
