View source for Vasomotion

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'''Vasomotion''' is the spontaneous oscillation in tone of [[blood vessel]]s, independent of [[Cardiac cycle|heart beat]], [[nerve|innervation]] or [[Respiration (physiology)|respiration]].<ref>Haddock RE, Hill CE. Rhythmicity in arterial smooth muscle. J Physiol (Lond ). 2005; 566:
645-656,Aalkaer C, Nilsson H. Vasomotion: cellular background for the oscillator and for the
synchronization of smooth muscle cells. Br J Pharmacol. 2005; 144: 605-616.</ref> While vasomotion was first observed by Jones in 1852, the complete mechanisms responsible for its generation and its physiological importance remain to be elucidated, however several hypothesis have been put forth.<ref>Aalkaer C, Nilsson H. Vasomotion: cellular background for the oscillator and for the
synchronization of smooth muscle cells. Br J Pharmacol. 2005; 144: 605-616.</ref>

==Mechanism==
Intercellular [[calcium]] (Ca<sup>2+</sup>) concentration exhibits periodic oscillations in vascular [[smooth muscle]] [[Cell (biology)|cell]]s, this is thought to be due Ca<sup>2+</sup> release from intercellular stores due to inositol tri-phosphate and ryanodine sensitive channel activation. This activation has been shown to result in either Ca<sup>2+</sup> "sparks", highly localized calcium increases, or "waves", global Ca<sup>2+</sup> increase that propagates the length of the cell.<ref>Jaggar JH, Porter VA, Lederer WJ, Nelson MT. Calcium sparks in smooth muscle. Am J Physiol Cell Physiol. 2000; 278: C235-256.</ref> To allow vasomotion to occur, synchronization must occur between the individual oscillations, resulting in global calcium synchronization and vessel tone oscillation.<ref>Nilsson H, Aalkjaer C. Vasomotion: mechanisms and physiological importance. Molecular Interventions. 2003; 3: 79-89.</ref>
[[Gap junction]]s 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.<ref>Haddock RE, Hirst GDS, Hill CE. Voltage independence of vasomotion in isolated irideal arterioles of the rat. J Physiol. 2002; 540: 219-229.</ref>.
Due to regional variations in gap junction distribution and coupling (homocellular vs. heterocellular) several hypothesis have been suggested to account for vasomotion occurrence. The "classic" mechanism of vasomotion generation is thought to be the voltage-dependent coupled model<ref>Nilsson H, Aalkjaer C. Vasomotion: mechanisms and physiological importance. Molecular
Interventions. 2003; 3: 79-89.</ref>. In this model, high gap junction coupling is present between the vascular smooth muscle cells, the [[Endothelium|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<ref>Parthimos D, Haddock RE, Hill CE, Griffith TM. Dynamics of A Three-Variable Nonlinear
Model of Vasomotion: Comparison of Theory and Experiment. Biophys J. 2007; 93: 1534-1556.</ref>. It is possible that in order for vasomotion to be generated, these systems must pass a depolarizing threshold.

==Physiological role==
Several possible hypothesis have been advanced to explain vasomotion. Increased flow is one possibility; mathematical modeling has shown a vessel with an oscillating diameter to conduct more flow then a vessel with a static diameter<ref>Meyer C, de Vries G, Davidge ST, Mayes DC. Reassessing the Mathematical Modeling of
the Contribution of Vasomotion to Vascular Resistance. J Appl Physiol. 2002; 92: 888-889.</ref>. Vasomotion could also be a mechanism of increasing the reactivity of a blood vessel by avoiding the "latch state", a low [[Adenosine triphosphate|ATP]] cycling state of prolonged force generation common in vascular smooth muscle. Finally, vasomotion has been shown to be altered in a variety of pathological situations, with vessels from both [[Hypertension|hypertensive]] and [[Diabetes mellitus|diabetic]] patients displaying altered flow patterns as compared to normotensive vessels<ref>Gratton RJ, Gandley RE, McCarthy JF, Michaluk WK, Slinker BK, McLaughlin MK.
Contribution of vasomotion to vascular resistance: a comparison of arteries from virgin and
pregnant rats. J Appl Physiol. 1998; 85: 2255-2260.</ref>.

==References==
{{Reflist}}

==See also==
* [[Vasoconstriction]]
* [[Vasodilation]]
* [[Vasospasm]]

{{cardiovascular_system}}
{{Cardiovascular physiology}}

[[Category:Cardiovascular system]]
[[Category:2Fix]]