Vasomotion - Mechanism


Intercellular calcium (Ca2+) concentration exhibits periodic oscillations in vascular smooth muscle cells, this is thought to be due Ca2+ release from intercellular stores due to inositol tri-phosphate and ryanodine sensitive channel activation. This activation has been shown to result in either Ca2+ "sparks", highly localized calcium increases, or "waves", global Ca2+ increase that propagates the length of the cell. To allow vasomotion to occur, synchronization must occur between the individual oscillations, resulting in global calcium synchronization and vessel tone oscillation. Gap junctions are thought to play a large role in this synchronization, as application of gap junction blockers has been shown to abolish vasomotion, indicating a critical role. Due to regional variations in gap junction distribution and coupling (homocellular vs. heterocellular) several hypotheses have been suggested to account for vasomotion occurrence. The "classic" mechanism of vasomotion generation is thought to be the voltage-dependent coupled model. In this model, high gap junction coupling is present between the vascular smooth muscle cells, the endothelial cells and the endothelial to vascular smooth muscle cells. An initial depolarizing current leads to the opening of the voltage dependent calcium channels, ultimately resulting in synchronization of individual calcium levels. When patch clamp recordings are conducted, depolarization occurs in the endothlial layer at the same time as the underlying vascular smooth muscle. The cause of the initial depolarizing current however remains to be determined, mathematical modeling has pointed to the existence of 2-4 independent non-linear oscillating systems interacting to produce vasomotion. It is possible that in order for vasomotion to be generated, these systems must pass a depolarizing threshold.

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