氯沙坦是一种特异性血管紧张素II受体拮抗剂，可增加离体大鼠后肢的血管紧张素I和血管紧张素II释放：血管组织中局部调节肾素-血管紧张素系统的证据。

Losartan, a specific angiotensin II receptor antagonist, increases angiotensin I and angiotensin II release from isolated rat hind legs: evidence for locally regulated renin-angiotensin system in vascular tissue.

作者信息

Mizuno K, Tani M, Niimura S, Sanada H, Haga H, Hashimoto S, Watanabe H, Ohtsuki M, Fukuchi S

机构信息

Third Department of Internal Medicine, Fukushima Medical College, Japan.

出版信息

Life Sci. 1992;50(23):PL209-14. doi: 10.1016/0024-3205(92)90070-6.

DOI:10.1016/0024-3205(92)90070-6

PMID:1598061

Abstract

The effect of Losartan (10(-9) to 10(-6) M) on angiotensins I and II release was examined in isolated hind legs perfused with Krebs-Ringer solution from normal and bilaterally nephrectomized rats. Losartan increased dramatically both angiotensins I (Ang I) and II (Ang II) release in a dose-dependent fashion; the maximal percent increment in Ang I and Ang II release evoked by Losartan (10(-6) M) was about +380% and +160%, respectively, in normal rat hind legs. In nephrectomized animals, Losartan elicited a marked increase in both peptides dose-dependently. There was a highly positive correlation between the released amounts of Ang I and that of Ang II altered by Losartan in either normal (r = 0.954) or nephrectomized rats (r = 0.923). These results not only confirm the existence of a functional renin-angiotensin system in vascular tissues, but also suggest that the system is regulated by locally generated Ang II.

摘要

在灌注来自正常大鼠和双侧肾切除大鼠的 Krebs-Ringer 溶液的离体后肢中，研究了氯沙坦（10⁻⁹至 10⁻⁶ M）对血管紧张素 I 和 II 释放的影响。氯沙坦以剂量依赖性方式显著增加血管紧张素 I（Ang I）和 II（Ang II）的释放；在正常大鼠后肢中，氯沙坦（10⁻⁶ M）引起的 Ang I 和 Ang II 释放的最大百分比增量分别约为 +380% 和 +160%。在肾切除的动物中，氯沙坦剂量依赖性地引起两种肽的显著增加。在正常（r = 0.954）或肾切除大鼠（r = 0.923）中，氯沙坦改变的 Ang I 释放量与 Ang II 释放量之间存在高度正相关。这些结果不仅证实了血管组织中存在功能性肾素 - 血管紧张素系统，还表明该系统受局部产生的 Ang II 调节。