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Am J Physiol Heart Circ Physiol 279: H3076-H3088, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H3076-H3088, December 2000

Slow intercellular Ca2+ signaling in wild-type and Cx43-null neonatal mouse cardiac myocytes

Sylvia O. Suadicani1,3, Monique J. Vink1, and David C. Spray1,2

1 Department of Neuroscience, 2 Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461; and 3 University São Judas Tadeu, São Paulo 03166, Brazil

Focal mechanical stimulation of single neonatal mouse cardiac myocytes in culture induced intercellular Ca2+ waves that propagated with mean velocities of ~14 µm/s, reaching ~80% of the cells in the field. Deletion of connexin43 (Cx43), the main cardiac gap junction channel protein, did not prevent communication of mechanically induced Ca2+ waves, although the velocity and number of cells communicated by the Ca2+ signal were significantly reduced. Similar effects were observed in wild-type cardiac myocytes treated with heptanol, a gap junction channel blocker. Fewer cells were involved in intercellular Ca2+ signaling in both wild-type and Cx43-null cultures in the presence of suramin, a P2-receptor blocker; blockage was more effective in Cx43-null than in wild-type cells. Thus gap junction channels provide the main pathway for communication of slow intercellular Ca2+ signals in wild-type neonatal mouse cardiac myocytes. Activation of P2-receptors induced by ATP release contributes a secondary, extracellular pathway for transmission of Ca2+ signals. The importance of such ATP-mediated Ca2+ signaling would be expected to be enhanced under ischemic conditions, when release of ATP is increased and gap junction channels conductance is significantly reduced.

calcium waves; connexin; gap junctions; purinergic receptors; intercellular communication


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