Hasegawa J, Hirai S, Kotake H, Hisatome I, Mashiba H
Department of Internal Medicine, Tottori University School of Medicine, Yonago, Japan.
Endocrinology. 1988 Dec;123(6):2805-11. doi: 10.1210/endo-123-6-2805.
The inotropic effect of the physiological level of TRH on isolated guinea pig cardiac muscle was studied using a force transducer and standard microelectrode techniques. TRH increased the contractile force of muscles dose-dependently without changing the time course of contraction in normal Tyrode and a high K+ (27 mM) solution. The positive inotropic effect of TRH was associated with an augmentation of slow action potentials in high K+ solution and was reduced in the presence of diltiazem, verapamil, and manganese. TRH potentiated the response of contractile force to increasing extracellular Ca2+ concentration. The inotropic effect of TRH was suppressed by metoclopramide, phentolamine, and cimetidine, but was not affected by propranolol. TRH increased the contractile force even in the myocardium of reserpinized guinea pig. It is suggested that TRH has a positive inotropic effect at least partly due to an increase in the slow inward Ca2+ current.
采用力传感器和标准微电极技术,研究了生理水平的促甲状腺激素释放激素(TRH)对离体豚鼠心肌的变力作用。在正常台氏液和高钾(27 mM)溶液中,TRH剂量依赖性地增加肌肉收缩力,而不改变收缩的时间进程。TRH的正性变力作用与高钾溶液中慢动作电位的增强有关,并且在存在地尔硫卓、维拉帕米和锰的情况下减弱。TRH增强了收缩力对细胞外Ca2+浓度升高的反应。甲氧氯普胺、酚妥拉明和西咪替丁抑制了TRH的变力作用,但普萘洛尔对其无影响。即使在利血平化豚鼠的心肌中,TRH也能增加收缩力。提示TRH具有正性变力作用,至少部分原因是慢内向Ca2+电流增加。