Inositol phosphate production following alpha 1-adrenergic, muscarinic or electrical stimulation in isolated rat heart.
A possible participation of polyphosphoinositide metabolism in the excitation-contraction coupling in heart was investigated. Isolated rat ventricles prelabelled with myo-[2-3H]inositol 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.
D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002851:Chromatography, High Pressure Liquid; D004558:Electric Stimulation; D005260:Female; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000096:biosynthesis*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000502:physiology*; D013403:Sugar Phosphates / Q000096:biosynthesis*; D010738:Type C Phospholipases / Q000378:metabolism
D007295:Inositol Phosphates; D011942:Receptors, Adrenergic, alpha; D011976:Receptors, Muscarinic; D013403:Sugar Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D002217:Carbachol; D010738:Type C Phospholipases; D009638:Norepinephrine