Previous studies suggest that the renal vasoconstrictor effect of angiotensin II (ANG II) is confined primarily to efferent arterioles, with little direct action on preglomerular vessels. The present study examined the role of prostaglandins (PG) in protecting preglomerular vessels from ANG II constriction. In dogs in which ANG II formation was blocked with captopril and renal artery pressure was servo-controlled, i.v. ANG II infusion (20 ng/kg per min) decreased renal blood flow (RBF) by about 50% while causing no significant change in glomerular filtration rate (GFR) and increasing filtration fraction (FF). After PG blockade, ANG II infusion decreased GFR by more than 30% and RBF by more than 50%, while causing much greater increases in calculated preglomerular resistance (RA) than in dogs without PG blockade. To prevent secondary changes in renal resistances via tubuloglomerular feedback (TGF), glomerular filtration was stopped by occluding the ureter during mannitol diuresis. After inhibition of TGF, ANG II decreased RBF markedly and increased glomerular hydrostatic pressure by 8-10 mmHg due to large increases in postglomerular resistance (RE) with no change in RA. After PG blockade and inhibition of TGF, ANG II decreased RBF by about the same amount as in control dogs but did not change glomerular hydrostatic pressure due to marked increases in both RA and RE. These data suggest that PGs selectively protect preglomerular vessels from ANG II constriction but do not interfere with the effect of ANG II on efferent arterioles.
Angiotensin II Animals