Vascular rhythmicity depends critically on calcium released from intracellular stores within smooth muscle cells and on cell coupling via gap junctions.
This review highlights that arterial vasomotion is driven by synchronized intracellular calcium release via gap junctions, distinguishing it from pacemaker-driven non-vascular smooth muscle.
Many arteries and arterioles exhibit rhythmical contractions which are synchronous over considerable distances. This vasomotion is likely to assist in tissue perfusion especially during periods of altered metabolism or perfusion pressure. While the mechanism underlying vascular rhythmicity has been investigated for many years, it has only been recently, with the advent of imaging techniques for visualizing intracellular calcium release, that significant advances have been made. These methods, when combined with mechanical and electrophysiological recordings, have demonstrated that the rhythm depends critically on calcium released from intracellular stores within the smooth muscle cells and on cell coupling via gap junctions to synchronize oscillations in calcium release amongst adjacent cells. While these factors are common to all vessels studied to date, the contribution of voltage-dependent channels and the endothelium varies amongst different vessels. The basic mechanism for rhythmical activity in arteries thus differs from its counterpart in non-vascular smooth muscle, where specific networks of pacemaker cells generate electrical potentials which drive activity within the otherwise quiescent muscle cells.
Haddock et al. (Fri,) conducted a review in Vascular rhythmicity (vasomotion). Vascular rhythmicity depends critically on calcium released from intracellular stores within smooth muscle cells and on cell coupling via gap junctions.