1. Although previous studies suggest that the renal vasoconstrictor effects of angiotensin II (ANG II) are normally confined to the efferent arterioles, the mechanisms that prevent ANG II from constricting preglomerular vessels are still unclear. In the present study, the role of prostaglandins (PG) in protecting preglomerular vessels from ANG II constriction was examined in dogs with normal or nonfiltering kidneys in which ANG II formation was blocked with captopril and renal artery pressure was servo-controlled at 75-80 mmHg. 2. Before PG blockade (n = 6), ANG II infusion (20 ng min-1 kg-1) decreased renal blood flow (RBF) by 54 ± 4%, but did not change glomerular filtration rate (GFR) significantly. After PG blockade (n = 6), ANG II infusion decreased GFR by 37 ± 7% and RBF by 56 ± 6%, while increasing calculated preglomerular resistance much more than before PG blockade. 3. In another group of dogs, secondary changes in renal resistances, due to tubuloglomerular feedback, were prevented by occluding the ureter during mannitol diuresis until glomerular filtration ceased. After inhibition of tubuloglomerular feedback in non-filtering kidneys (n = 7), ANG II decreased RBF by 40 ± 3% and increased glomerular hydrostatic pressure, estimated from stop-flow ureteral pressure and plasma colloid osmotic pressure, by 8.7 ± 1.7 mmHg. Postglomerular resistance increased by 91 ± 12% while preglomerular resistance was unchanged. After PG blockade and inhibition of tubuloglomerular feedback (n = 7), ANG II decreased RBF by 43 ± 4%, but did not change glomerular hydrostatic pressure due to large increases in both preglomerular (125 ± 46%) and postglomerular (81 ± 19%) resistance. 4. These observations suggest that with physiological increases in ANG II levels, PG minimize reductions in GFR by preventing preglomerular constriction without interfering with the effect of ANG II on postglomerular vessels.
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