As blood flow is proportional to the fourth power of the vascular radius small changes in the diameter of resistance arteries/arterioles following an increase in intraluminal pressure would be expected to substantially increase blood flow. However, arteriolar myocytes display an intrinsic ability to locally regulate blood flow according to metabolic demands by tuning the diameter of small arteries in response to local changes in he-modynamics. Critical to this, observations were made more than 100 years ago that mechanosensitive small arteries exhibit the "myogenic response" or pressure-induced vasoconstriction or vasodilation in re-sponse to increased or decreased intravascular pressure, respectively. Although cellular mechanisms underlying the myogenic response have now been studied extensively, the precise cellular mechanisms under-lying this intriguing phenomenon still remain uncertain. In particular, the biological machinery that senses changes in intravascular pressure in vascular smooth muscle cells have not been unquestionably identified and remain a significant issue in vascular biology to be fully elucidated. As such, this brief review focuses on putative mechanosensors that have been proposed to contribute to myogenic vasoreactivity. Specific attention is paid to the roles of integrins, G protein-coupled receptors, and cadherins.
Keywords: Cadherins; G protein-coupled receptor; Integrins; Pressure-induced vasoconstriction/vasodilation.
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