Katz A M
Department of Medicine, University of Connecticut, Farmington 06032.
Circulation. 1990 Aug;82(2 Suppl):I7-11.
beta-Adrenergic agonists and other agents that increase cellular levels of cyclic adenosine monophosphate (cyclic AMP) exert complex actions on myocardial cell function that enhance both the force of contraction and the rate of relaxation. At the same time that cyclic AMP increases the amount of activator Ca2+ released at the onset of systole, which increases contractility, this intracellular messenger accelerates the removal of activator Ca2+ from the cytosol by the sarcoplasmic reticulum, which promotes relaxation. Cyclic AMP also increases Ca2+ sensitivity of the sarcoplasmic reticular Ca2+ pump and desensitizes contractile proteins to Ca2+, both of which favor relaxation. Thus, the lusitropic effects of cyclic AMP, which allow the heart to remove increased amounts of activator Ca2+ from the cytosol, occur simultaneously with cyclic AMP's inotropic effects. This interplay between inotropic and lusitropic effects allows beta-adrenergic agonists to increase myocardial contractility while accelerating relaxation, a combination of effects that allows the ventricles to fill during the agonist-induced tachycardia.
β-肾上腺素能激动剂和其他增加细胞内环磷酸腺苷（cAMP）水平的药物，对心肌细胞功能具有复杂的作用，既能增强收缩力，又能加快舒张速率。在cAMP增加收缩期开始时释放的激活剂Ca2+量从而增加收缩性的同时，这种细胞内信使通过肌浆网加速激活剂Ca2+从细胞质中的清除，这促进了舒张。cAMP还增加肌浆网Ca2+泵对Ca2+的敏感性，并使收缩蛋白对Ca2+脱敏，这两者都有利于舒张。因此，cAMP的变时性作用使心脏能够从细胞质中清除增加量的激活剂Ca2+，与cAMP的变力性作用同时发生。变力性和变时性作用之间的这种相互作用使β-肾上腺素能激动剂在加速舒张的同时增加心肌收缩力，这种联合作用使心室在激动剂诱导的心动过速期间能够充盈。
