title: Differential mechanisms involved in effects of genistein and 17-beta-estradiol on porcine coronary arteries.
abstract: The purpose of this work was to examine the differential mechanisms involved in relaxation induced by genistein and 17-beta-estradiol in isolated porcine coronary arteries. Similar to 17-beta-estradiol, genistein could dose-dependently relax 30 mM KCI-precontracted coronary artery rings. The pD2 values of genistein and 17-beta-estradiol were 4.91 +/- 0.13 and 4.98 +/- 0.12 respectively. Incubation with N-L-nitroarginine (L-NNA), endothelium removal or in the presence of a potent inhibitor of protein tyrosine phosphatase sodium orthovanadate did not affect the relaxation induced by genistein, but could partially reduce the vasorelaxation induced by 17-beta-estradiol. The relaxations induced by genistein and 17-beta-estradiol were unaffected by the estrogen receptor antagonist tamoxifen, the inhibitor of prostanoid synthesis indomethacin and the protein synthesis inhibitor, cycloheximide. In addition, both of genistein and 17-beta-estradiol could decrease the contractile responses of KCI, 5-HT and CaCl2, and shift their cumulative concentration-response curves rightward in a parallel manner. These findings suggest that the relaxant effects induced by genistein and 17-beta-estradiol are probably mainly due to inhibition of Ca2+ influx through voltage-dependent calcium channels (VDCCs), and are not related to sex hormone receptor and classical genomic activities. Also there is an interesting finding that the relaxing response of 17-beta-estradiol is partially endothelium-dependent, but that of genistein is not.
authors.affiliation: Department of Physiology, College of Basic Medicine, Lanzhou University, People's Republic of China. lihf@lzu.edu.cn
authors.forename: Hong-Fang
authors.initials: HF
authors.lastname: Li
authors.forename: Peng
authors.initials: P
authors.lastname: Zhang
authors.forename: Zhi-Feng
authors.initials: ZF
authors.lastname: Tian
authors.forename: Xiao-Qing
authors.initials: XQ
authors.lastname: Qiu
authors.forename: Ying-Fu
authors.initials: YF
authors.lastname: Zhang
authors.forename: Jin-Xia
authors.initials: JX
authors.lastname: Wu
authors.forename: Zhong-Jian
authors.initials: ZJ
authors.lastname: Jia
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002118:Calcium / Q000502:physiology; D002122:Calcium Chloride / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D019833:Genistein / Q000494:pharmacology*; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D011189:Potassium Chloride / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism; D013552:Swine
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D004965:Estrogen Antagonists; D011448:Prostaglandin Antagonists; D011500:Protein Synthesis Inhibitors; D012701:Serotonin; D004958:Estradiol; D011189:Potassium Chloride; D019833:Genistein; D002122:Calcium Chloride; D002118:Calcium