Pulmonary Edema Induced by Angiotensin I in Rats

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Author(s)

    • Xu Zhe-Hu XU Zhe-Hu
    • Department of Preventive Medicine, Division of Social Medicine, Medical Research Institute, Tokyo Medical and Dental University
    • WANG Li-Man
    • Department of Preventive Medicine, Division of Social Medicine, Medical Research Institute, Tokyo Medical and Dental University
    • MINESHITA Satoru
    • Department of Preventive Medicine, Division of Social Medicine, Medical Research Institute, Tokyo Medical and Dental University

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 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.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 76(1), 51-56, 1998-01

    The Japanese Pharmacological Society

References:  26

Cited by:  1

Codes

  • NII Article ID (NAID)
    10008191097
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    00215198
  • NDL Article ID
    4395857
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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