Zhe-Hu Xu, Kazuro Shimakura, Takatsugu Yamamoto, Li-Man Wang and Satoru
Mineshita
Department of Preventive Medicine, Division of Social Medicine, Medical
Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima,
Bunkyo-ku, Tokyo 113, Japan
Abstract: 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 microg/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 alpha-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 microg/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.
Keywords: Pulmonary edema, Angiotensin I, Angiotensin converting enzyme,
Losartan, Phentolamine