Genistein treatment reduces arterial contractions by inhibiting tyrosine kinases in ovariectomized hypertensive rats

被引:21
作者
Nevala, R
Lassila, M
Finckenberg, P
Paukku, K
Korpela, R
Vapaatalo, H
机构
[1] Univ Helsinki, Inst Biomed, Biomedicum, Dept Pharmacol & Toxicol, FIN-00014 Helsinki, Finland
[2] Univ Helsinki, Dept Virol, Haartman Inst, FIN-00014 Helsinki, Finland
基金
芬兰科学院;
关键词
genistein; estradiol-17; beta; SHR (spontaneously hypertensive rat); renal artery; tyrosine phosphorylation;
D O I
10.1016/S0014-2999(02)02270-7
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The aim of the present study was to evaluate the vascular effects of genistein in a short-term study. The ovariectomized spontaneously hypertensive rats (SHR) were divided into four groups (n = 8 in each), which received the following subcutaneous treatments either for 2 days or for 2 weeks: (1) solvent control (96% dimethylsulphoxide (DMSO) 1 ml/kg), (2) estradiol-17beta (25 mug/kg), (3) genistein (2.5 mg/kg; low-dose), and (4) genistein (25 mg/kg; high-dose). The renal arterial rings were studied using organ bath system. The renal artery contractions were attenuated by the 2-day low-dose genistein treatment as follows: angiotensin II (46%), noradrenaline (42%) KCl (36%), and endothelin-1 (34%). Only the angiotensin II-induced contractions were reduced by the 2-week treatment with estradiol-17beta (38%) and with the low-dose of genistein (31%). The 2-day genistein treatment reduced tyrosine phosphorylation, while the other treatments or treatment times had no effect. The 2-day low-dose genistein treatment had no estrogenic effect on the uterine morphology. The mechanism for attenuated contractility in the renal arteries after the 2-day low-dose genistein treatment is independent of the estrogenic effect of genistein, but is due to the tyrosine kinase inhibitory property of genistein. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:87 / 96
页数:10
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