Ca2+ regulation of connexin 43 hemichannels in C6 glioma and glial cells

Connexin-43 Hemichannels Mediate Cyclic ADP-ribose Generation and Its Ca2+-mobilizing Activity by NAD+/Cyclic ADP-ribose Transport

“…The rapid decline of [Ca 2ϩ ] i after a rise could be mediated by rapid Cx 43 closing, which might be a negative feedback loop in regulation of [Ca 2ϩ ] i . This is supported by the reports that Cx43 opening is negatively regulated by intracellular Ca 2ϩ (31). In addition, Cx43 permeability is negatively regulated by PKC which is activated by the elevation of [ ] i is cADPR whose production and delivery to its action site is tightly regulated by the Cx43/CD38 system.…”

At the cross-point of connexins, calcium, and ATP: blocking hemichannels inhibits vasoconstriction of rat small mesenteric arteries

“…While moderate ( 500 nM) [Ca 2þ ] i elevation stimulates hemichannel opening, most likely via calmodulin signalling, [6][7][8] larger (500-1000 nM) [Ca 2þ ] i increases result in hemichannel closure, presumably via actomyosin contraction that disrupts loop-tail interaction. 37 Our unitary current data demonstrate that CT9 prevents high [Ca 2þ ] i closure of Cx43-hemichannels.…”

“…Hemichannels are permeable to Ca 2þ and may thus contribute to cellular Ca 2þ entry 4 and diffusive ATP release. 5 Moreover, hemichannel opening is [Ca 2þ ] i -dependent in a bimodal manner, [6][7][8][9][10] with moderate [Ca 2þ ] i elevation favouring opening and above $500 nM [Ca 2þ ] i inhibiting opening. The bimodal Ca 2þ -dependence of hemichannels resembles the Ca 2þ -dependence of inositol-trisphosphate receptor (IP 3 R) channels, which are Ca 2þ release channels in the endoplasmic reticulum (ER) that play a central role in generating Ca 2þ oscillations in diverse cell types including SMCs.…”

Chemistry, Physiology, and Pharmacology of β.-Adrenergic Mechanisms in the Heart. Why are .β-Blocker Antiarrhythmics Superior?

“…Partial uncoupling of gap junctions prior to ischaemia by ischemic-preconditioning preserves the electrical coupling of cells during a subsequent ischemic insult, indicating that a partial closure of gap junctions may play a trigger role in the protection [94,96,154,155]. GAP26 and GAP27 blocks calcium-triggered ATP release mediated by Cx43 hemichannels [156][157][158][159]. Hemichannels are not engaged to gap junctions, and they are open under several physiological and pathophysiological conditions [160].…”