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.
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