Smooth muscle contraction is regulated by changes in cytosolic Ca(2+) concentration ([Ca(2+)](i)). In response to stimulation, Ca(2+) increase in a single cell can propagate to neighbouring cells through gap junctions, as intercellular Ca(2+) waves. To investigate the mechanisms underlying Ca(2+) wave propagation between smooth muscle cells, we used primary cultured rat mesenteric smooth muscle cells (pSMCs). Cells were aligned with the microcontact printing technique and a single pSMC was locally stimulated by mechanical stimulation or by microejection of KCl. Mechanical stimulation evoked two distinct Ca(2+) waves: (1) a fast wave (2mm/s) that propagated to all neighbouring cells, and (2) a slow wave (20μm/s) that was spatially limited in propagation. KCl induced only fast Ca(2+) waves of the same velocity as the mechanically induced fast waves. Inhibition of gap junctions, voltage-operated calcium channels, inositol 1,4,5-trisphosphate (IP(3)) and ryanodine receptors, shows that the fast wave was due to gap junction mediated membrane depolarization and subsequent Ca(2+) influx through voltage-operated Ca(2+) channels, whereas, the slow wave was due to Ca(2+) release primarily through IP(3) receptors. Altogether, these results indicate that temporally and spatially distinct mechanisms allow intercellular communication between SMCs. In intact arteries this may allow fine tuning of vessel tone.
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