Angiotensin II receptors in rabbit renal preglomerular vessels

Controversy exists regarding the specific sites within the renal microcirculation affected by angiotensin II (ANG II). Under some conditions, ANG II can elicit direct vasoconstrictor responses in the preglomerular vessels and efferent arterioles. These experiments were designed to evaluate the binding of ¹²⁵I-ANG II in preglomerular vessels. Arcuate and interlobular arteries, with attached proximal segments of afferent arterioles, were microdissected from rabbit renal cortexes. A membrane preparation was obtained from the pooled freshly dissected vessels and utilized in an ANG II radioreceptor assay on the same day. Binding site concentrations [N] and dissociation constants [K(D)] were obtained by Scatchard analyses of binding inhibition data. Specific binding was saturable and reversible. The dissociation of bound ANG II was enhanced in the presence of a nonhydrolyzable analogue of GTP. Linear Scatchard plots were obtained, indicating the presence of a single class of high-affinity binding sites. The K(D) and N are similar to those for ANG II receptors in extrarenal vascular tissue. The order of binding inhibition potencies of ANG analogues was [Sar¹,Ile⁸]-ANG II >> [Sar¹,Ala⁸] ANG II = ANG II = ANG III >>> ANG I, which is consistent with in vivo observations of the effects of these analogues on renal blood flow. The binding inhibition potencies of ANG III and [Sar¹,Ile⁸]ANG II were greater in renal compared with reported values for extrarenal vasculature and rabbit glomeruli. Furthermore, there were no differences in ANG II receptor parameters in preglomerular vessels obtained from pregnant and nonpregnant rabbits. This contrasts to that previously observed in rabbit glomeruli, suggesting that intrarenal vascular and glomerular receptors may differ. In conclusion, there is a single class of specific ANG II receptors in preglomerular vessels. The K(D) and N are similar, but the binding inhibition potencies of selected ANG analogues differ in renal and extrarenal vascular tissues. Intrarenal vascular receptors also appear to differ from glomerular receptors. Furthermore, these data support the concept that ANG II may affect renal vascular resistance at sites proximal to the distal afferent arterioles.