An Official Journal of the American Heart Association Actions of Adenosine and Isoproterenol on Isolated Mammalian Ventricular Myocytes
An Official Journal of the American Heart Association Actions of Adenosine and Isoproterenol on Isolated Mammalian Ventricular Myocytes
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发表时间：
2005
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通讯作者：
L. Belardinelli;G. Isenberg
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作者：
L. Belardinelli;G. Isenberg
我们研究了腺苷和异丙肾上腺素对牛和豚鼠心室肌细胞酶分散的影响。细胞内刺激具有规则的刺激模式和正常静息电位的松弛的肌细胞导致伴随收缩的完全平台的动作电位。浓度高达0.2 HIM的腺苷对任何动作电位参数或基础收缩力均无显著影响。相反，在相同的细胞中，腺苷有效地拮抗异丙肾上腺素的刺激作用。异丙肾上腺素（1-10 nM）延长了34- 41%的动作电位，将平台置换为更正的电位，并导致肌细胞肌节缩短程度增加3倍。在存在腺苷（5-50 HM）的情况下，异丙肾上腺素仅使动作电位时程增加8- 9%，平台期的移动几乎消失，肌细胞肌节缩短程度的增加不到10%。在一些心肌细胞中，异丙肾上腺素（1-10 nM）诱导去极化后电位伴随后收缩。后除极偶尔达到阈值，导致触发持续的节律性活动。腺苷（20-50 μ M）不仅使后除极和后收缩的幅度减小，而且使持续的节律活动消失。我们的结论是：第一，分离的心室肌细胞对异丙肾上腺素和腺苷有反应;第二，腺苷没有直接的作用，但能有效地拮抗异丙肾上腺素的刺激作用;第三，研究结果与多细胞心室制备的结果一致;第四步，减弱异丙肾上腺素作用所需的腺苷浓度在心脏细胞释放的腺苷浓度范围内当氧可用性有限和/或需求增加时;以及第五，内源性释放的腺苷可以调节儿茶酚胺的电生理和收缩作用。(Circ Res 53：287-297，1983）
We investigated the effects of adenosine and isoproterenol on enzymatically dispersed ventricular myocytes from bovine and guinea pig hearts. Inrracellular stimulation of relaxed myocytes with regular srriation patterns and normal resting potential resulted in action potentials with full plateaus accompanied by contractions. Adenosine in concentrations up to 0.2 HIM had no significant effect on any of the action potential parameters or on the basal contractility. In contrast, in the same cells, adenosine effectively antagonized the stimulatory effect of isoproterenol. Isoproterenol (1-10 nM) prolonged the action potentials by 34-41%, displaced the plateau to more positive potentials, and caused a 3-fold increase in the extent of myocyte sarcomere shortening. In the presence of adenosine (5-50 HM), isoproterenol increased the action potential duration by only 8-9%, the shift of the plateau was nearly abolished, and the increase in the extent of myocyte sarcomere shortening was less than 10%. In some of the myocytes, isoproterenol (1-10 nM) induced depolarizing afterpotentials accompanied by aftercontractions. The afterdepolarizations occasionally reached threshold resulting in triggered sustained rhythmic activity. Adenosine (20-50 HM) not only reduced the amplitude of the afterdepolarizarions and aftercontractions, but also abolished the sustained rhythmic activity. We conclude, first, that isolated ventricular myocytes respond to isoproterenol and adenosine; second, that adenosine has no direct effect, but effectively antagonizes the stimulatory actions of isoproterenol; third, that findings are consistent with the ones reported for multicellular ventricular preparations; fourth, that adenosine concentrations required to attenuate the actions of isoproterenol are in the range of adenosine concentrations released by cardiac cells when oxygen availability is limited and/or demand is increased; and fifth, that endogenously released adenosine may modulate the electrophysiological and contractile effects of catecholamines. (Circ Res 53: 287-297, 1983)