Roles of focal adhesion and cytoskeleton dynamics in myogenic vascular regulation
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Ligand-dependent or ligand-independent activation of ion channels or G-protein-coupled receptors contributes to pressure-induced vasoconstriction or vasodilation critical for the maintenance of blood flow response to the physiological alternation of intravascular pressures (e.g., elevation of arterial intraluminal pressure leading to vasoconstriction). A mechanosensitive integrin-dependent focal adhesion complex rearranges cytoskeletal structures for myogenic responsiveness in vascular smooth muscle cells. Myogenic responses maintain blood flow, generate vascular tone, prevent damage to capillaries due to high blood pressure, and reduce edema caused by high capillary hydrostatic pressure. However, enhanced myogenic vasoconstriction causes cardiovascular diseases (e.g., hypertension and vasospasm). Thus, small arteries and arterioles may be equipped with negative regulatory mechanisms to prevent exaggerated myogenic responses. Overall, the studies described in this mini literature review aim to explain that pressure (stretch)-dependent vasoconstriction is controlled by mechanisms underlying negative feedback regulation regarding focal adhesion molecules or cytoskeletons. Since the development of therapeutic approaches for the negative regulations of myogenic vasoconstriction helps overcome vascular disorders, this review focuses on myogenic vascular regulation and its negative feedback mechanisms.
Abstract
Ligand-dependent or ligand-independent activation of ion channels or G-protein-coupled receptors contributes to pressure-induced vasoconstriction or vasodilation critical for the maintenance of blood flow response to the physiological alternation of intravascular pressures (e.g., elevation of arterial intraluminal pressure leading to vasoconstriction). A mechanosensitive integrin-dependent focal adhesion complex rearranges cytoskeletal structures for myogenic responsiveness in vascular smooth muscle cells. Myogenic responses maintain blood flow, generate vascular tone, prevent damage to capillaries due to high blood pressure, and reduce edema caused by high capillary hydrostatic pressure. However, enhanced myogenic vasoconstriction causes cardiovascular diseases (e.g., hypertension and vasospasm). Thus, small arteries and arterioles may be equipped with negative regulatory mechanisms to prevent exaggerated myogenic responses. Overall, the studies described in this mini literature review aim to explain that pressure (stretch)-dependent vasoconstriction is controlled by mechanisms underlying negative feedback regulation regarding focal adhesion molecules or cytoskeletons. Since the development of therapeutic approaches for the negative regulations of myogenic vasoconstriction helps overcome vascular disorders, this review focuses on myogenic vascular regulation and its negative feedback mechanisms.
참고문헌 (21)
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