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1 Microvascular Biology Group, School of Medical Sciences, RMIT University, Bundoora, Victoria 3083, Australia; 2 Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655; and 3 Cardiovascular Research Institute, Department of Medical Physiology, College of Medicine, Texas A&M University, College Station, Texas 77843
The smooth muscle of arterioles responds to an increase in intraluminal pressure with vasoconstriction and with vasodilation when pressure is decreased. Such myogenic vasoconstriction provides a level of basal tone that enables arterioles to appropriately adjust diameter in response to neurohumoral stimuli. Key in this process of mechanotransduction is the role of changes in intracellular Ca2+. However, it is becoming clear that considerable complexity exists in the spatiotemporal characteristics of the Ca2+ signal and that changes in intracellular Ca2+ may play roles other than direct effects on the contractile process via activation of myosin light-chain phosphorylation. The involvement of Ca2+ may extend to modulation of ion channels and release of Ca2+ from the sarcoplasmic reticulum, alterations in Ca2+ sensitivity, and coupling between cells within the vessel wall. The purpose of this brief review is to summarize the current literature relating to Ca2+ and the arteriolar myogenic response. Consideration is given to coupling of Ca2+ changes to the mechanical stimuli, sources of Ca2+, involvement of ion channels, and spatiotemporal aspects of intracellular Ca2+ signaling.
arterioles; myogenic response; calcium entry; calcium signaling
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