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A possible participation of polyphosphoinositide metabolism in the excitation-contraction coupling in heart was investigated. Isolated rat ventricles prelabelled with myo-2-3Hinositol were stimulated by conditions that increase mechanical activity. Both noradrenaline and carbachol increased the basal level of IP3, IP2 and IP by the activation of alpha 1-adrenergic and muscarinic receptors, respectively. Electrical stimulation accelerated inositol lipid degradation by phospholipase C thus enhancing the IP3 level as compared to quiescent ventricles. It is proposed that IP3 may be involved in excitation-contraction coupling in cardiac tissue.
Poggioli et al. (1986) studied this question.
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