Abstract
Many of the cardiovascular parameters or incidences of coronary artery diseases display circadian variations. These day/night time variances may be attributable to the diurnal change in vascular contractility. However, the molecular mechanism of the vascular clock system which generates the circadian variation of vascular contractility has remained largely unknown. Recently we found the existence of the intrinsic circadian rhythm in vascular contractility. A clock gene Rorα in vascular smooth muscle cells (VSMC) provokes the diurnal oscillatory change in the expression of Rho-associated kinase 2 (ROCK2), which induces the time-of-day-dependent variation in the agonist-induced phosphorylation of myosin light chain (MLC) and myofilament Ca2+ sensitization. In this review, we introduce our recent findings with reference to the molecular basis of the biological clock system and the current literature concerning cardiovascular chronobiology.
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