| First Author | Yamazaki D | Year | 2011 |
| Journal | Cell Metab | Volume | 14 |
| Issue | 2 | Pages | 231-41 |
| PubMed ID | 21803293 | Mgi Jnum | J:176728 |
| Mgi Id | MGI:5292583 | Doi | 10.1016/j.cmet.2011.05.011 |
| Citation | Yamazaki D, et al. (2011) TRIC-A channels in vascular smooth muscle contribute to blood pressure maintenance. Cell Metab 14(2):231-41 |
| abstractText | TRIC channel subtypes, namely TRIC-A and TRIC-B, are intracellular monovalent cation channels postulated to mediate counter-ion movements facilitating physiological Ca(2+) release from internal stores. Tric-a-knockout mice developed hypertension during the daytime due to enhanced myogenic tone in resistance arteries. There are two Ca(2+) release mechanisms in vascular smooth muscle cells (VSMCs); incidental opening of ryanodine receptors (RyRs) generates local Ca(2+) sparks to induce hyperpolarization, while agonist-induced activation of inositol trisphosphate receptors (IP(3)Rs) evokes global Ca(2+) transients causing contraction. Tric-a gene ablation inhibited RyR-mediated hyperpolarization signaling to stimulate voltage-dependent Ca(2+) influx, and adversely enhanced IP(3)R-mediated Ca(2+) transients by overloading Ca(2+) stores in VSMCs. Moreover, association analysis identified single-nucleotide polymorphisms (SNPs) around the human TRIC-A gene that increase hypertension risk and restrict the efficiency of antihypertensive drugs. Therefore, TRIC-A channels contribute to maintaining blood pressure, while TRIC-A SNPs could provide biomarkers for constitutional diagnosis and personalized medical treatment of essential hypertension. |
