Chen J, Zhang L F, Han C, Yu G S, Ma J
Department of Aerospace Physiology, The Fourth Military Medical University, P.R. China.
J Gravit Physiol. 1996 Apr;3(1):57-62.
We have previously demonstrated that prolonged simulated microgravity (tail-suspension) leads to cardiac alterations with increased resting heart rate, myocardial degradation changes and attenuated myocardial contractility. The present study investigated the potential role of adrenoceptor mechanisms underlying them. Changes of myocardial alpha 1-adrenoceptor (alpha 1-AR) and beta 1-adrenoceptor (beta-AR) in 90-day tail-suspended rats was investigated by the method of radioligand binding assay and application of Scatchard's method. The results showed significantly decreased quantity of specific binding of 125I-BE[2-beta-(4-hydroxy-3-[125I]indophenyl)-ethylaminomethyltetralone] to alpha 1-AR present in membrane derived from ventricular myocardium of the suspended animals, despite the affinity of the alpha 1-AR to 125I-Be was unchanged. But neither the quantity nor the affinity of beta-AR binding to 125I-Pindolol was significantly altered. In addition, the spontaneously beating rate of isolated right atria from tail-suspended animals showed little change in sensitivity and reactivity to the stimulations of graded phenylephrine (alpha-agonist, measured in the presence of beta-antagonist propranolol) and isoproterenol (beta-agonist), compared with the control rats. There were also no obvious differences of the effects of the isoproterenol on the contractility of isolated left ventricular papillary muscles between the two groups. Since myocardial alpha 1-AR mediated-effects include production of cardiac hypertrophy and enhancement of myocardial glucose uptake and glycolysis, the down-regulation of the alpha 1-AR may be a contributor to the cardiac cellular accumulation and the myocardial degradation changes as found in our tail-suspended rats. The data from this study also suggest that the myocardial beta-adrenoceptors are not affected by the prolonged tail-suspension.
我们之前已经证明，长时间模拟微重力（尾部悬吊）会导致心脏改变，表现为静息心率增加、心肌降解变化以及心肌收缩力减弱。本研究调查了其潜在的肾上腺素能受体机制。通过放射性配体结合测定法和应用Scatchard方法，研究了90天尾部悬吊大鼠心肌α1-肾上腺素能受体（α1-AR）和β1-肾上腺素能受体（β-AR）的变化。结果显示，尽管α1-AR对125I-Be的亲和力未变，但与悬吊动物心室肌膜中存在的α1-AR特异性结合的125I-BE[2-β-(4-羟基-3-[125I]吲哚苯基)-乙基氨基甲基四氢萘酮]的数量显著减少。但是β-AR与125I-吲哚洛尔结合的数量和亲和力均未发生显著改变。此外，与对照大鼠相比，尾部悬吊动物分离的右心房自发搏动率对分级去氧肾上腺素（α-激动剂，在β-拮抗剂普萘洛尔存在下测量）和异丙肾上腺素（β-激动剂）刺激的敏感性和反应性变化不大。两组之间异丙肾上腺素对分离的左心室乳头肌收缩力的影响也没有明显差异。由于心肌α1-AR介导的效应包括心脏肥大的产生以及心肌葡萄糖摄取和糖酵解的增强，α1-AR的下调可能是导致我们尾部悬吊大鼠心脏细胞堆积和心肌降解变化的一个因素。本研究的数据还表明，心肌β-肾上腺素能受体不受长时间尾部悬吊的影响。
