Excitation-contraction coupling in rested-state contractions of guinea-pig ventricular myocardium.
Different types of rested-state contractions were examined under the influence of various inotropic agents. In magnesium-free solution, in low sodium (40 mmol/l) solution or in the presence of dihydroouabain, an "early" rested-state contraction developed without delay after stimulation. A distinctive "late" rested-state contraction was observed under the influence of noradrenaline. It is characterized by a latent period of about 100 ms between stimulation and onset of contraction. This latency was not reduced by increasing the catecholamine concentration, despite a concentration-dependent increase in the height of the "late" rested-state contraction. The late rested-state contraction under the influence of noradrenaline was suppressed by the slow inward current inhibitor nifedipine whether or not the nifedipine-dependent shortening of the action potential duration was prevented by caesium. When the slow inward current was not inhibited, the prolongation of the action potential duration by caesium resulted in an increase of the late rested-state contraction because of a prolongation of the time to peak force. High concentrations of dihydroouabain led to the appearance of an early contraction component without appreciably influencing the noradrenaline-dependent late component. From this it was deduced that the activator calcium for the late rested-state contraction was not stored intracellularly during rest prior to stimulation and, consequently, could not have been released by inflowing calcium. Instead, it is proposed that the activator calcium for the late rested-state contraction entered the sites of the sarcoplasmic reticulum and subsequently released from its release sites as long as the cell was depolarized. The "early" rested-state contractions in Mg2+-free solution, in low sodium solution or in the presence of dihydroouabain were not influenced in their contraction velocity by high concentrations of nifedipine which fully inhibited the late rested-state contractions. Nifedipine caused only a slight reduction in peak force due to a shortening of the time to peak force as a result of a shortening in action potential duration. This indicates that the activator calcium for the "early" rested-state contractions had accumulated in the sarcoplasmic reticulum during rest prior to stimulation and that it was released immediately by depolarization without a participation of the slow inward current.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002586:Cesium / Q000494:pharmacology; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D066298:In Vitro Techniques; D008274:Magnesium / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects*; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010042:Ouabain / Q000031:analogs & derivatives / Q000494:pharmacology; D010210:Papillary Muscles / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D012964:Sodium / Q000502:physiology
C000977:dihydroouabain; D002586:Cesium; D010042:Ouabain; D012964:Sodium; D008274:Magnesium; D009543:Nifedipine; D002118:Calcium; D009638:Norepinephrine