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Effect of methylprednisolone on recovery of beta-adrenergic desensitization in rat hearts.

作者信息

Sugiyama S, Hayashi K, Hanaki Y, Taki K, Ozawa T

机构信息

Department of Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Japan.

出版信息

Arzneimittelforschung. 1991 Apr;41(4):439-43.

PMID:1650227
Abstract

The effects of methylprednisolone (Solu-Medrol, CAS 83-43-2) on isoprenaline (isoproterenol)-induced decreases in the number of beta-receptors and adenylate cyclase activities in rat hearts. Rats were divided into 4 groups: 1. the control group, untreated; 2. the ISPOd group; 3. the ISP7d group, 10 mg/kg of isoprenaline was subsequently injected once a day for 6 successive days, and rats were cervically dislocated 15 h or 7 days after the last isoprenaline injection, respectively; 4. the ISP + MP7d group, 20 mg/kg of methylprednisolone was intraperitoneally injected once a day for 7 successive days following 6 successive days of isoprenaline injection, and rats were cervically dislocated. A significant decrease in the number of beta-receptors was observed (28.9 +/- 4.2 fmol/mg protein) after 6 successive isoprenaline injections compared with the control (41.7 +/- 3.6), and this significant decrease persisted for 7 days (32.6 +/- 5.8). Administration of methylprednisolone accelerated the recovery of beta-receptors (38.4 +/- 5.1) 7 days after the last isoprenaline injection. Adenylate cyclase activities were also decreased by successive isoprenaline treatments (isoprenaline-stimulated adenylate cyclase activity, 13.9 +/- 2.7 pmol/min/mg protein; basal adenylate cyclase activity, 11.2 +/- 1.7) compared with the control (isoprenaline-stimulated, 25.7 +/- 3.7; basal, 18.1 +/- 2.4). Significant decreases in adenylate cyclase activities were observed 7 days after isoprenaline administration (isoprenaline-stimulated, 17.7 +/- 3.9; basal, 14.8 +/- 2.4). Methylprednisolone also accelerated the recoveries (isoprenaline-stimulated, 20.3 +/- 2.9; basal, 17.1 +/- 3.9). These results indicate that methylprednisolone accelerated the recovery of the decrease in beta-adrenergic responsiveness caused by successive administrations of isoprenaline.

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