Angiotensin II: preferential efferent constriction?

In dogs with maximal subpression of endogenous angiotensin II (AII) production due to a high-salt diet and converting enzyme inhibition (CEI, SQ 14,225, 15 micrograms X kg-1 X min-1 i.v.), infusion of a subpressor dose of angiotensin II (1 ng X kg-1 X min-1) did not change contralateral kidney function. In the infused kidney, a decrease in renal blood (RBF) by 24% and glomerular filtration rate (GFR) by 9% with an increase in filtration fraction (FF) by 20% occurred. Similarly, the increase in single nephron (SN) RBF was greater than in SNGFR, thus rising SNFF by 8%. Glomerular capillary pressure (GCP) did not change significantly; a decrease by 20% in proximal tubule pressure thus resulted in an increase in delta HP by 22%. This increase counterbalanced the profound drop in ultrafiltration coefficient (Kf) (57%) making the decrease in GFR and SNGFR relatively small. Total arteriolar resistance (RT) rose by 26%, the rise being due mainly to an increase in efferent (RE, 50%) rather than afferent (RA, 4%) resistance. If the AII infusion was carried out during concomitant infusion of CEI and indomethacin (1 mg X kg-1 X min-1) or aspirin (5 mg X kg-1 X min-1), RBF decreased by 36%, GFR by 25%, thus increasing FF by 18%; corresponding SN values underwent similar changes. Drop in Kf amounted to 62% and hydraulic pressure difference (delta HP) increased by 11% with unchanged GCP. The increase in RT (72%) was now due to a very similar increase in both RA (68%) and RE (76%). In conclusion, a very small dose of AII exhibits-at least in superficial nephrons-a typical preferential efferent effect which disappears after inhibition of prostanoid synthesis, indicating a protective effect of vasodilatory prostaglandins mainly on the afferent arteriole.