Pulmonary Edema Induced by Angiotensin I in Rats

The Japanese Journal of Pharmacology

Satoru Mineshita¹  Kazuro Shimakura¹  Li-Man Wang¹  Takatsugu Yamamoto¹  Zhe-Hu Xu¹ 

[1] Department of Preventive Medicine, Division of Social Medicine, Medical Research Institute, Tokyo Medical and Dental University

关键词: Pulmonary edema;    Angiotensin I;    Angiotensin converting enzyme;    Losartan;    Phentolamine;   

DOI  :  10.1254/jjp.76.51

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(26)Cited-By(7)This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 μg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an α-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 μg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.

【 授权许可】

Unknown