Ca-release by phosphoinositides from sarcoplasmic reticulum of frog skeletal muscle.
To clarify the biological role of phosphoinositides including inositol trisphosphate (IP3) in the skeletal muscle, we examined the Ca-releasing action on the heavy fraction of sarcoplasmic reticulum (HFSR) from bullfrog skeletal muscle of IP3, phosphatidylinositol monophosphate (PIP), phosphatidylinositol 4,5-bisphosphate (PIP2), and glycerophosphoinositol 4,5-bisphosphate (GPIP2). Only PIP2 caused dose-dependent Ca release. IP3 (up to 55 microM), PIP (up to 37 microM), and GPIP2 (up to 33 microM) were ineffective. The PIP2-induced Ca release is due to the direct action of PIP2, but not its metabolite(s). The properties of the PIP2-induced Ca release are unique and cannot be accounted for by the Ca release mechanisms already reported, such as Ca2+-induced, ionic substitution-induced, or IP3-induced Ca release. The rate of the PIP2-induced Ca release, however, is so slow that it may have no physiological relevance unless stimulating factors or agents exist.
Ogawa
Y
Y
Department of Pharmacology, Juntendo University School of Medicine, Tokyo.
Harafuji
H
H
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D066298:In Vitro Techniques; D019269:Phosphatidylinositol 4,5-Diphosphate; D010716:Phosphatidylinositols / Q000037:antagonists & inhibitors / Q000502:physiology*; D011892:Rana catesbeiana; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*
D019269:Phosphatidylinositol 4,5-Diphosphate; D010716:Phosphatidylinositols; D002118:Calcium