ROLE OF KININS AND ANGIOTENSIN-II IN THE VASODILATING ACTION OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION IN RAT RENAL VESSELS

Objective To assess directly the vasodilating effects of angiotensin c onverting enzyme (ACE) inhibition in different renal vessels and to de termine the role of kinins and angiotensin II (ANGII) therein, Methods Lumen diameters of different vessels and glomerular blood flows were measured in cortical and juxtamedullary glomeruli by in-vivo microscop y in the split hydronephrotic kidney of anesthetized female Wistar rat s. Results Injection of the ACE inhibitor quinapril at a dose of 0.9 m g/kg intravenously, which blocks conversion of locally applied angiote nsin I (1 mu mol/l), increased glomerular blood flows by 39 +/- 6 and 18 +/- 4% in cortical and juxtamedullary glomeruli, respectively, due to vasodilatation in all renal vessels, The most pronounced vasodilata tion was observed in interlobular arteries (19 +/- 2%) and in cortical afferent arterioles (16 +/- 3%). Pretreatment of the hydronephrotic k idney by local application of 40 nmol/l Hoe140, a bradykinin B-2 recep tor antagonist, or 3 mu mol/l valsartan, an ANGII type 1 receptor anta gonist, attenuated the vasodilatation in response to quinapril, ANGII receptor blockade affected only weakly, whereas bradykinin receptor bl ockade blunted markedly, the quinapril-induced vasodilatation, suggest ing that kinins play an important role in our experimental model, Admi nistration of valsartan, which abrogated the renal vasoconstriction in duced by 10 nmol/l ANGII completely, caused vasodilatation of magnitud e similar to that caused by administration of quinapril, Yet, the vaso dilatation induced by the combination of valsartan and quinapril was s ignificantly larger than that induced by administration of quinapril a lone in interlobular arteries, afferent arterioles, and cortical effer ent arterioles, Conclusions Our results indicate that kinins and ANGII can contribute to the renal vasodilatation in response to ACE inhibit ors, but ACE inhibitors appear to have only minor effects on ANGII lev els in those renal vessels, which are the well-known sites of renin ex pression.