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Rescue Effect of Exercise on Impaired Arteriolar Myogenic Response with Advancing Age

이만균|홍광석
한국운동생리학회|2017.02|운동과학 (Exercise Science)|제26권 제1호|pp. 8-16|DOI 10.15857/ksep.2017.26.1.8

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참고문헌

키워드

AgingProtein kinase CVascular smooth muscle cellsMyogenic reactivityPressure-induced vasoconstriction

초록

PURPOSE: Mechanosensitive vascular smooth muscle cells (VSMCs) of resistance arteries crucially regulate blood flow by constricting or dilating over fluctuation of blood pressure (the myogenic response). This review was aimed at introducing cellular signaling that is relevant to arterial myogenic response and briefly describing how the arterial autoregulation is impaired by aging and exercise intervention restores the diminished myogenic responsiveness. METHODS: A systemic literature research was conducted through PUBMED to comprehend previous studies that explore molecular mechanisms underlying arterial myogenic response, impaired pressure-induced vasoconstriction with advancing age, and effect of exercise training on the arterial autoregulation. RESULTS: The myogenic response generally consists of three steps: 1) detection of mechanical stress (e.g. stretch, tension) exerted on VSMCs, 2) biological transduction pathways (e.g., depolarization, Ca2+ entry, phosphorylation of myosin light chain, Ca2+ sensitization, actin polymerization), and 3) adjustment of vascular tone (e.g. vasoconstriction or dilation). Aging induces vascular aging that is coupled to increased risks of development of cardiovascular diseases. The intrinsic ability of VSMCs to maintain appropriate blood flow in response to changes in intravascular pressure has been reported to be impaired with advancing age. In contrast, exercise intervention has been demonstrated to rescue aging-induced attenuation of arterial myogenic responsiveness. CONCLUSIONS: Abnormal myogenic response of resistance arteries leads to vascular rupture, vasospasms, hypertension, or hypotension. Therefore, it will be valuable to investigate the exact mechanisms underlying the contribution of exercise training to arterial myogenic response to prevent and treat impaired arterial autoregulation-induced cardiovascular disorders.

Abstract

PURPOSE: Mechanosensitive vascular smooth muscle cells (VSMCs) of resistance arteries crucially regulate blood flow by constricting or dilating over fluctuation of blood pressure (the myogenic response). This review was aimed at introducing cellular signaling that is relevant to arterial myogenic response and briefly describing how the arterial autoregulation is impaired by aging and exercise intervention restores the diminished myogenic responsiveness. METHODS: A systemic literature research was conducted through PUBMED to comprehend previous studies that explore molecular mechanisms underlying arterial myogenic response, impaired pressure-induced vasoconstriction with advancing age, and effect of exercise training on the arterial autoregulation. RESULTS: The myogenic response generally consists of three steps: 1) detection of mechanical stress (e.g. stretch, tension) exerted on VSMCs, 2) biological transduction pathways (e.g., depolarization, Ca2+ entry, phosphorylation of myosin light chain, Ca2+ sensitization, actin polymerization), and 3) adjustment of vascular tone (e.g. vasoconstriction or dilation). Aging induces vascular aging that is coupled to increased risks of development of cardiovascular diseases. The intrinsic ability of VSMCs to maintain appropriate blood flow in response to changes in intravascular pressure has been reported to be impaired with advancing age. In contrast, exercise intervention has been demonstrated to rescue aging-induced attenuation of arterial myogenic responsiveness. CONCLUSIONS: Abnormal myogenic response of resistance arteries leads to vascular rupture, vasospasms, hypertension, or hypotension. Therefore, it will be valuable to investigate the exact mechanisms underlying the contribution of exercise training to arterial myogenic response to prevent and treat impaired arterial autoregulation-induced cardiovascular disorders.

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