ANGIOTENSIN-II AND RENAL PROSTAGLANDIN RELEASE IN THE DOG - INTERACTIONS IN CONTROLLING RENAL BLOOD-FLOW AND GLOMERULAR-FILTRATION RATE

The relationship between angiotensin II and renal prostaglandins, and their interactions in controlling renal blood flow (RBF) and glomerula r filtration rate (GFR) were investigated in 18 anaesthetized dogs wit h acutely denervated kidneys. Intrarenal angiotensin II infusion incre ased renal PGE, release (veno-arterial concentration difference times renal plasma flow) from 1.7 +/- 0.9 to 9.1 +/- 0.4 and 6-keto-PGF(1) a lpha release from 0.1 +/- 0.1 to 5.3 +/- 2.1 pmol min(-1). An angioten sin II induced reduction in RBF of 20% did not measurably change GFR w hereas a 30% reduction reduced GFR by 18+/-8%. Blockade of prostagland in synthesis approximately doubled the vasoconstrictory action of angi otensin II, and all reductions in RBF were accompanied by parallel red uctions in GFR. When prostaglandin release was stimulated by infusion of arachidonic acid (46.8 +/- 13.3 and 15.9 +/- 5.4 pmol min(-1) for P GE(2), and 6-keto-PGF(1) alpha, respectively), angiotensin II did not change prostaglandin release, but had similar effects on the relations hip between RBF and GFR as during control. In an ureteral occlusion mo del with stopped glomerular filtration measurements of ureteral pressu re and intrarenal venous pressure permitted calculations of afferent a nd efferent vascular resistances. Until RBF was reduced by 25-30% angi otensin II increased both afferent and efferent resistances almost equ ally, keeping the ureteral pressure constant. At greater reductions in RBF, afferent resistance increased more than the efferent leading to reductions in ureteral pressure. This pattern was not changed by block ade of prostaglandin synthesis indicating no influence of prostaglandi ns on the distribution of afferent and efferent Vascular resistances d uring angiotensin II infusion. In this ureteral occlusion model glomer ular effects of angiotensin II mill not be detected, and it might well be that the shift from an effect predominantly on RBF to a combined e ffect on both RBF and GFR induced by inhibition of prostaglandin synth esis is located to the glomerulus. We therefore postulate that renal p rostaglandins attenuate the effects of angiotensin II on glomerular su rface area and the filtration barrier, and not on the afferent arterio les as previously suggested.