日本生理学会大会発表要旨集
日本生理学会大会発表要旨集
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ラット肥大心の酸素消費増加におけるNCXの役割
*伊藤 治男清水 壽一郎松岡 達金 鳳柱竹内 綾子中島ー竹中 千香子山下 大輔坂田 進高木 都
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The aim of the present study was to prove the different energetics in isoproterenol-induced hypertrophied hearts compared to normal hearts. Myocardial O2 consumption per minute (mVO2) in myocardial slices was measured without and with 1-Hz field stimulation (stim.). mVO2 without stim. corresponds to basal metabolic mVO2. Delta mVO2 (= mVO2 with stim.-mVO2without stim.) corresponds to O2 consumption in excitation-contraction (E-C) coupling. Basal metabolic mVO2 was significantly smaller but delta mVO2 was significantly larger in the hypertrophy. Na+-Ca2+ exchange (NCX1) current was markedly increased associated with depressed sarcoplasmic reticulum Ca2+ ATPase (SERCA2) activity due to decreased phospho-Ser16 phospholamban expression, resulting in the increase of delta mVO2. Since the NCX1 protein expression level did not increase, the marked increase in NCX1 current is attributable, at least in part, to attenuation of the intrinsic inactivation mechanisms of NCX1. It is plausible that decreased basal metabolic mVO2 is due to depressed Na+/K+ ATPase (NKA) expression and/or activity because of phospholemman overexpression in this hypertrophy. However, measured NKA current was not decreased. We concluded that the different origin of the O2 consumption in E-C coupling in the hypertrophy was derived from decreased SERCA2 activity (1ATP: 2Ca2+) and increased NCX activity coupled to NKA activity (1ATP: Ca2+). [J Physiol Sci. 2008;58 Suppl:S184]
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© 2008 日本生理学会
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