アブストラクト（27巻1号：The Bulletin of Kanagawa Dental College）

The Bulletin of Kanagawa Dental College

English

Title　： Effects of Nitric Oxide (NO) Released from NO Donor NOC-7 on Myofilament Contractility in Skinned Rabbit Myocardiac Trabeculae
Subtitle　： Selective Proceedings of 33rd General Meeting of Kanagawa Odontological Society, 1998
Authors　： Shun-suke Takahashi, Hirofumi Shoji, Eiichiro Okabe
Authors（kana）　：
Organization　： Department of Pharmacology and ESR Laboratory, Kanagawa Dental College
Journal　： The Bulletin of Kanagawa Dental College
Volume　： 27
Number　： 1
Page　： 73-75
Year/Month　： 1999 / 3
Article　： Report
Publisher　： Kanagawa Odontological Society
Abstract　： [Abstract] The aim of this study is to determine the direct effect of nitric oxide (NO) released from NO donor 3-(2-hydroxy-1-methylethyl-2-nitrosohydrazino)-N-methyl-1-propanamine (NOC-7), on the myocardial contractile function. In electron spin resonance study, NO released from NOC-7 was detected as NO-DTCS-Fe2+ spin adduct, which was increased in a time-dependent fashion up to 1 hr. NOC-7 decreased both myofilament Ca2+ -sensitivity and hill coefficient, the binding cooprativity between troponin C and Ca2+, in a concentration-dependent manner. NOC-7 also produced an increase in rigor tension obtained in pCa 9.03 solution in the absence of ATP, in a concentration-dependent fashion. Myofibrillar-bound creatine kinase activity determined as rigor tension obtained in pCa 9.03 solution containing creatine phosphate in the absence of ATP was decreased by NOC-7. It is suggested that NO can reduce myocardial contractile function and that crossbridge behavior may be affected by NO. Our results also consistent with the view that these alterations in contractile properties of myocardium induced by NO appear to be due to the inhibition of creatine kinase activity, suggesting that the observed effect of NO may be mediated via inhibition of rephosphorylation of ADP to ATP.
Practice　： Dentistry
Keywords　： Nitric oxide, Electron spin resonance, Myocardiac filament Ca2+ sensitivity, Crossbridge, Creatine kinase activity