Key result
Ionophore X537-A increased cardiac muscle contractility by 67% in the presence of external calcium, but was completely ineffective in producing a positive inotropic effect in the absence of external calcium.
The positive inotropic effect of ionophore X537-A in cardiac muscle is dependent on extracellular calcium transport across the sarcolemma rather than intracellular release alone.
Highlights extracellular calcium dependence for inotropy; leaves open translation to human therapeutics or ionophore development.
The role of extracellular calcium in the positive inotropic effect of X537-A in dog's cardiac muscle was investigated. Ionophore (20 mug/ml) in the presence of external calcium increased the contractility by 67 +/- 12 percent within 2 min. In the absence of external calcium ionophore was ineffective in producing a positive inotropic effect in the muscle. Lanthanum, an inhibitor of calcium influx, in the concentrations of 2, 4, 6, and 8 mM produced a concentration dependent decrease in the contractility. Ionophore-induced increase in the contractility was inversely related to the concentration of lanthanum used. It is suggested that the release of calcium from intracellular stores under the effect of ionophore is not enough to maintain contractility. Also positive inotropic effect of ionophore appears to be mediated through the transportation of calcium across the sarcolemma. Such ionophore mediated transportation of calcium appears to be dependent upon surface binding of calcium.
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Singal et al. (1976) studied Normal cardiac muscle. Ionophore X537-A vs. Calcium-free solution and Lanthanum was evaluated on Force of contraction (contractility) (67 ± 12 percent increase). Ionophore X537-A increased cardiac muscle contractility by 67% in the presence of external calcium, but was completely ineffective in producing a positive inotropic effect in the absence of external calcium.
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