Hamada K
Second Department of Internal Medicine, Toho University School of Medicine, Tokyo, Japan.
Nihon Jinzo Gakkai Shi. 2001;43(1):28-34.
In the present study, the role of the angiotensin II type 2 receptor in the regulation of medullary blood flow in conscious Spontaneous Hypertensive Rats(SHR) was investigated. We tested the hypothesis that AT2 receptor activation may exert the opposite effects of AT1 receptors in terms of renal hemodynamics. Mean arterial pressure(MAP), daily sodium balance, cortical blood flow(CBF), and medullary blood flow(MBF) were measured over a 10-day protocol in several groups of rats in which optical fibers for laser-Doppler flowmetry had been implanted and which received the following drug combinations: the AT1 receptor antagonist CV11976(CV) alone and CV plus AT2 receptor antagonist PD123319 (PD). In the CV alone group, the renal interstitial administration of CV decreased MAP, caused sodium diuresis, and increased MBF significantly. In the CV plus PD group, the renal interstitial administration of PD prevented sustained hypotension, sodium diuresis, and increased medullary blood flow during CV administration. These data indicated that AT2 receptor activation leads to vasodilation in the renal medulla and an antihypertensive effect in SHR. AT2 receptors play an important role in the renal medullary blood flow.
在本研究中，我们研究了2型血管紧张素受体在清醒自发性高血压大鼠（SHR）髓质血流调节中的作用。我们检验了这样一个假设，即就肾脏血流动力学而言，AT2受体激活可能产生与AT1受体相反的作用。在几组大鼠中，通过为期10天的实验方案测量平均动脉压（MAP）、每日钠平衡、皮质血流（CBF）和髓质血流（MBF）。这些大鼠已植入用于激光多普勒血流测定的光纤，并接受以下药物组合：单独使用AT1受体拮抗剂CV11976（CV）以及CV加AT2受体拮抗剂PD123319（PD）。在单独使用CV组中，经肾间质给予CV可降低MAP、引起钠利尿，并显著增加MBF。在CV加PD组中，经肾间质给予PD可防止在给予CV期间出现持续性低血压、钠利尿以及髓质血流增加。这些数据表明，AT2受体激活可导致肾髓质血管舒张，并在SHR中产生降压作用。AT2受体在肾髓质血流中起重要作用。
