title: [TRIC(trimeric intracellular cation)-A channels contribute to blood pressure maintenance in vascular smooth muscle].
abstract: TRIC (trimeric intracellular cation) channel subtypes, namely TRIC-A and TRIC-B, are intracellular monovalent cation channels postulated to mediate counter-ion movements facilitating physiological Ca²⁺ release from intracellular stores. Tric-a-knockout mice developed hypertension during the daytime due to enhanced myogenic tone in resistance arteries. There are two Ca²⁺ release mechanisms in vascular smooth muscle cells (VSMCs); incidental opening of ryanodine receptors (RyRs) generates local Ca²⁺ sparks to induce hyperpolarization, while agonist-induced activation of inositol trisphosphate receptors (IP₃Rs) evokes global Ca²⁺ transients causing contraction. Tric-a gene ablation inhibited RyR-mediated hyperpolarization signaling to stimulate voltage-dependent Ca²⁺ influx, and adversely enhanced IP₃R-mediated Ca²⁺ transients by overloading Ca²⁺ stores in VSMCs. Therefore, TRIC-A channels contribute to maintaining blood pressure in vascular smooth muscles.
authors.affiliation: Department of Biological Chemistry, Graduate School of Phamaceutical Sciences, Kyoto University, Japan. daiju-y@pharm.kyoto-u.ac.jp
authors.forename: Daiju
authors.initials: D
authors.lastname: Yamazaki
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D007473:Ion Channels / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009131:Muscle, Smooth, Vascular / Q000502:physiology*
chemical_list: D007473:Ion Channels; C522221:TRIC-A protein, mouse; C522222:TRIC-B protein, mouse; D002118:Calcium