The Effect Of Angiotensin Ii On Afferent Arteriolar Function

Using microperfused renal afferent (Af) and efferent arterioles (Ef), we examined the actions of angiotensin II (AII) on these arterioles. All caused dose-dependent constriction of both arterioles in rabbits; however, the sensitivity was higher in the Ef. The constriction was blocked with All type 1 receptor antagonist (AT(1)R-A), whereas it was augmented with AT(2) RA. Selective activation of AT(2) R in Af resulted in vasodilation, which was abolished by either disrupting the endothelium or inhibiting the synthesis of epoxyeicosatrienoic acid (EET). This dilation was impaired in the spontaneously hypertensive rats (SHR). Thus, AT(1)R mediates Af and Ef vasoconstriction, whereas activation of AT(2) R may cause vasodilation via endothelial production of EETs. In SHR Af, AII causes exaggerated vasoconstriction possibly due to altered AT(2) R function.