To assess directly the vasodilating effects of angiotensin converting enzyme (ACE) inhibition in different renal vessels and to determine 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 microscopy in the split hydronephrotic kidney of anesthetized female Wistar rats.Results
Injection of the ACE inhibitor quinapril at a dose of 0.9 mg/kg intravenously, which blocks conversion of locally applied angiotensin I (1 μmol/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 vasodilatation was observed in interlobular arteries (19 ± 2%) and in cortical afferent arterioles (16 ± 3%). Pretreatment of the hydronephrotic kidney by local application of 40 nmol/l Hoe140, a bradykinin B2 receptor antagonist, or 3 μmol/l valsartan, an ANGII type 1 receptor antagonist, attenuated the vasodilatation in response to quinapril. ANGII receptor blockade affected only weakly, whereas bradykinin receptor blockade blunted markedly, the quinapril-induced vasodilatation, suggesting that kinins play an important role in our experimental model. Administration of valsartan, which abrogated the renal vasoconstriction induced by 10 nmol/l ANGII completely, caused vasodilatation of magnitude similar to that caused by administration of quinapril. Yet, the vasodilatation induced by the combination of valsartan and quinapril was significantly larger than that induced by administration of quinapril alone in interlobular arteries, afferent arterioles, and cortical efferent arterioles.Conclusions
Our results indicate that kinins and ANGII can contribute to the renal vasodilatation in response to ACE inhibitors, but ACE inhibitors appear to have only minor effects on ANGII levels in those renal vessels, which are the well-known sites of renin expression.