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The rate of the spontaneous activity of cultured cells from the chick embryonic ventricle was only slightly increased by norepinephrine (NE) or epinephrine (EP), even if it was applied close to the cell. On the other hand, the amplitude of contraction, measured from the shortening of the diameter of the cell aggregate, was clearly augmented by up to 50%. Intracellularly injected cAMP also potentiated contraction. Namely, NE, EP, or cAMP showed positive inotropic action but slight chronotropic action on cultured ventricle cells. NE produced an increase in the action potential amplitude, shortening of action potential, and slight hyperpolarization in 17- to 19-day-old but not in 7- to 9-day-old embryo. If NE was applied to the cells whose plateau potential was inhibited by the previous treatment with nifedipine, NE recovered the plateau level to the control. Iontophoretically injected cAMP also recovered the plateau level once it had been inhibited by nifedipine or verapamil. In some cells, the membrane was transiently depolarized after the end of injection and turned back to the control level. This transient depolarization took place spontaneously again. It was suggested that the Ca2+-induced Ca2+ release mechanism from the sarcoplasmic reticulum was involved in the cyclic depolarization.

Differentiation of inotropic action from chronotropic action of sympathetic agents in cultured cells of chick embryonic ventricles.