Huang C L, Davis G, Johns E J
Department of Physiology, Medical School, Birmingham.
Exp Physiol. 1991 Sep;76(5):787-98. doi: 10.1113/expphysiol.1991.sp003544.
The effect of angiotensin II on blood pressure and perfusion of blood through the cortex and papilla regions of the kidney was determined in pentobarbitone-anaesthetized rats which were subjected to laser-Doppler flowmetry to estimate regional renal haemodynamics. Angiotensin II was infused at 10, 45 and 150 ng (kg body weight-1 min-1) which caused dose-related increases in blood pressure of 3, 12 and 24%, respectively, and decreases in cortical perfusion of 9, 15 and 24%, respectively. Papillary perfusion did not change at any dose of angiotensin II. This pattern and magnitude of responses to angiotensin II in blood pressure, cortical and papillary perfusions was essentially unaffected (a) following blockade of cyclo-oxygenase activity with indomethacin (1.3 mg kg-1 plus 2 mg kg-1 h-1), (b) during infusion of a bradykinin antagonist, at 1.3 micrograms min-1, (c) when renal perfusion pressure was regulated at control levels and (d) following Methylene Blue administration to inhibit potential endothelial-derived relaxing factor production. By contrast, infusion of phenylephrine at 5, 10 and 20 micrograms kg-1 min-1 caused dose-related increases in blood pressure and decreases in both cortical and papillary perfusions reaching some 28, 7 and 17% respectively at the highest dose of phenylephrine used. These results showed that both cortex and papilla were sensitive to vasoconstrictor agents. They are compatible with the suggestion that angiotensin II regulates cortical but not papillary perfusion in the kidney, and that these responses do not depend on prostaglandin, bradykinin, renal perfusion pressure or endothelium-derived relaxing factor.
在戊巴比妥麻醉的大鼠中，通过激光多普勒血流仪测定肾皮质和乳头区的血流动力学，以确定血管紧张素II对血压以及肾脏皮质和乳头区血液灌注的影响。分别以10、45和150 ng/（kg体重·分钟）的剂量输注血管紧张素II，导致血压分别升高3%、12%和24%，皮质灌注分别降低9%、15%和24%。在任何血管紧张素II剂量下，乳头灌注均未改变。血管紧张素II在血压、皮质和乳头灌注方面的这种反应模式和幅度，在以下情况下基本不受影响：（a）用吲哚美辛（1.3 mg/kg加2 mg/kg·小时）阻断环氧化酶活性后；（b）以1.3 μg/分钟的剂量输注缓激肽拮抗剂期间；（c）将肾灌注压调节至对照水平时；（d）给予亚甲蓝以抑制潜在的内皮源性舒张因子产生后。相比之下，分别以5、10和20 μg/（kg体重·分钟）的剂量输注去氧肾上腺素，导致血压呈剂量依赖性升高，皮质和乳头灌注均降低，在所用去氧肾上腺素的最高剂量下分别达到约28%、7%和17%。这些结果表明，皮质和乳头对血管收缩剂均敏感。它们与以下观点一致：血管紧张素II调节肾脏皮质而非乳头的灌注，且这些反应不依赖于前列腺素、缓激肽、肾灌注压或内皮源性舒张因子。
