Longitudinal smooth muscle of the mammalian intestine. A model for Ca2+ signaling by cADPR
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Updated: Oct 31, 2026

Applications of Spatio-temporal Mapping and Particle Analysis Techniques to Quantify Intracellular Ca2+ Signaling In Situ
Published on: January 7, 2019
J F Kuemmerle1, K S Murthy, G M Makhlouf
1Department of Physiology, Medical College of Virginia, Richmond 23298-0711, USA.
Abstract:
Ca2+ mobilization in muscle cells from the circular muscle layer of the mammalian intestine is mediated by IP3-dependent Ca2+ release. Ca2+ mobilization in muscle from the adjacent longitudinal muscle layer involves a distinct, phosphoinositide-independent pathway. Receptors for contractile agonists in longitudinal muscle cells are coupled via a pertussis toxin-sensitive G protein to activation of PLA2 and formation of arachidonic acid (AA). The latter activates Cl- channels resulting in depolarization of the plasma membrane and opening of voltage-sensitive Ca2+ channels. Ca2+ influx via these channels induces Ca2+ release by activating sarcoplasmic ryanodine receptor/Ca2+ channels. The increase in [Ca2+]i activates membrane-bound ADP ribosyl cyclase, and the resultant formation of cADPR enhances Ca(2+)-induced Ca2+ release.
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