Endlich K, Steinhausen M
Department of Anatomy and Cell Biology I, University of Heidelberg Germany.
J Hypertens. 1997 Jun;15(6):633-41. doi: 10.1097/00004872-199715060-00010.
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.
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.
Injection of the ACE inhibitor quinapril at a dose of 0.9 mg/kg intravenously, which blocks conversion of locally applied angiotensin I (1 mumol/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 mumol/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 vasodilation 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.
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.
直接评估血管紧张素转换酶（ACE）抑制对不同肾血管的舒张作用，并确定激肽和血管紧张素II（ANGII）在其中的作用。
通过体内显微镜测量麻醉的雌性Wistar大鼠分侧肾积水肾脏皮质和近髓肾小体中不同血管的管腔直径和肾小球血流量。
静脉注射剂量为0.9mg/kg的ACE抑制剂喹那普利，可阻断局部应用的血管紧张素I（1μmol/l）的转化，由于所有肾血管的舒张，皮质和近髓肾小体的肾小球血流量分别增加39±6%和18±4%。在小叶间动脉（19±2%）和皮质传入小动脉（16±3%）中观察到最明显的血管舒张。通过局部应用40nmol/l Hoe140（一种缓激肽B2受体拮抗剂）或3μmol/l缬沙坦（一种ANGII 1型受体拮抗剂）对肾积水肾脏进行预处理，可减弱对喹那普利的血管舒张反应。ANGII受体阻断作用较弱，而缓激肽受体阻断则明显减弱喹那普利诱导的血管舒张，表明激肽在我们的实验模型中起重要作用。缬沙坦可完全消除10nmol/l ANGII诱导的肾血管收缩，其引起的血管舒张程度与喹那普利相似。然而，缬沙坦和喹那普利联合诱导的血管舒张在小叶间动脉、传入小动脉和皮质传出小动脉中明显大于单独使用喹那普利诱导的血管舒张。
我们的结果表明，激肽和ANGII可促成ACE抑制剂引起的肾血管舒张，但ACE抑制剂似乎对那些肾素表达的著名部位的肾血管中ANGII水平只有轻微影响。
