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Local elementary purinergic-induced Ca2+ transients: from optical mapping of nerve activity to local Ca2+ signaling networks

The Journal of General Physiology
The Rockefeller University Press
Publication Date
DOI: 10.1085/jgp.201010402
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The Rockefeller University Press $30.00 J. Gen. Physiol. Vol. 136 No. 2 149–154 149 P e r s p e c t i v e The autonomic nervous system regulates smooth muscle contractility through both sympathetic and parasympa- thetic influences. In some tissues, such as the urinary bladder, parasympathetic influences predominate and nerves communicate to detrusor smooth muscle through the release of acetylcholine (ACh). In other tissues, such as the vas deferens and mesenteric arterial circula- tion, the primary autonomic influence is sympathetic, and norepinephrine (NE) is the predominant neurotrans- mitter. NE and ACh act on smooth muscle cells through Gq-coupled -adrenergic and muscarinic receptors, re- spectively, which signal through PLC to elevate diacyl- glycerol and inositol trisphosphate (IP3), which in turn, activate PKC and IP3 receptors (IP3Rs) in the SR. IP3-mediated Ca2+ release from the SR of vascular smooth muscle cells gives rise to Ca2+ waves (Iino and Tsukioka, 1994; Jaggar and Nelson, 2000; Wray et al., 2005; Kim et al., 2008), which are propagating elevations in Ca2+ that are thought to contribute to vascular smooth mus- cle contraction (Mauban et al., 2001; Zang et al., 2006). The consequences of G protein–coupled signaling events manifest after a characteristic lag, reflecting the temporal dynamics of multiple sequential and parallel molecular linkages. Although NE and ACh are the prototypical transmit- ters released by autonomic nerves, it has long been known that ATP is coreleased with NE at sympathetic nerve–muscular junctions and with ACh at parasympa- thetic nerve–muscular junctions. Coreleased ATP acts on P2X receptor channels in the plasma membrane of smooth muscle cells. Because P2X receptors are ion channels, once activated, their effects are experienced almost immediately by the cell. This rapid time course is in contrast to the more delayed influence of the G protein–coupled adrenergic and muscarin

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