Abstract
Plasma membrane inositol phospholipids were breakdown by hormones and neurotransmitters through the mediation of the specific receptors (1–4). This phosphatidylinositol (PI) turnover pathway generates two second messengers, inositol-(l,4,5)-trisphosphate (IP3) and sn-1,2-diacylglycerol (DAG) (5,6). DAG stimulates membrane-bound phospholipid-dependent, Ca2+- dependent protein kinase C (7), while IP3 releases Ca2+ from stores in the sarcoplasmic reticulum (8,9). The physiological significance of this Pi–turnover pathway is not still clear in any mammalian cell system. It is controversial whether IP3 stimulates Ca2+ release from SR in cardiac myocytes.
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© 1992 Springer-Verlag Tokyo
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Kawaguchi, H. et al. (1992). PI Response and Calcium Overload in Cardiomyopathic Hamster Heart Cell. In: Yasuda, H., Kawaguchi, H. (eds) New Aspects in the Treatment of Failing Heart. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68219-6_7
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DOI: https://doi.org/10.1007/978-4-431-68219-6_7
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-68221-9
Online ISBN: 978-4-431-68219-6
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