Pulmonary Edema Induced by Angiotensin II in Rats.

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  • Shimakura Kazuro
    <I>Department of Preventive Medicine, Medical Research Institute, Tokyo Medical and Dental University</I>
  • Sanaka Masaki
    <I>Department of Preventive Medicine, Medical Research Institute, Tokyo Medical and Dental University</I>
  • Wang Li-man
    <I>Department of Preventive Medicine, Medical Research Institute, Tokyo Medical and Dental University</I>
  • Mineshita Satoru
    <I>Department of Preventive Medicine, Medical Research Institute, Tokyo Medical and Dental University</I>
  • Miyazaki Mizuo
    <I>Department of Pharmacology, Osaka Medical College</I>

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We performed this study to demonstrate the experimental procedure for inducing pulmonary edema by angiotensin II (AT II) in rats and to determine the mechanism of hemodynamic pulmonary edema. In the pilot study, 10 μg/ml of AT II was found to be adequate as the edematogenic dose for inducing pulmonary edema. The edematogenic dose of AT II was intravenously given to rats pretreated with 20 mg/kg of an AT II-receptor antagonist, E 4177 (3-[(2''-carboxybiphenyl-4-yl)methyl]-2-cyclopropyl-7-methyl-3H-imidazo[4, 5-b]pyridine), and to rats given 10 mg/kg of an alpha-adrenergic blocker, phentolamine. Similarly, pulmonary edema was induced by 25 μg/ml of adrenaline in rats pretreated with E 4177 (20 mg/kg) and rats with no pretreatment. E 4177 completely suppressed the development of AT II-induced pulmonary edema, whereas phentolamine could not. On the contrary, E 4177 could not suppress the development of adrenaline-induced pulmonary edema. We concluded that AT II-induced pulmonary edema will develop via the specific AT II receptor without the indirect action of adrenaline.

収録刊行物

  • Jpn.J.Pharmacol.

    Jpn.J.Pharmacol. 67 (4), 383-389, 1995

    公益社団法人 日本薬理学会

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