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- W2018892856 abstract "TRIC (trimeric intracellular cation) channels in the sarco-/endoplasmic reticulum likely act as counter-ion channels that conduct monovalent cations in a synchronized manner with release of stored Ca2+. TRIC channel subtypes display differential expression patterns as TRIC-A is predominantly expressed in excitable tissues, including brain and muscle, and TRIC-B is present throughout many tissues. TRIC-A knockout mice are viable and fertile, while TRIC-B knockout mice exhibit neonatal lethality due to respiratory failure (Yamazaki et al., Development 2009), and double-knockout mice lacking both subtypes show embryonic cardiac failure (Yazawa et al., Nature, 2007). To resolve the physiological role of TRIC-A, we are currently focusing on abnormal circulatory function in TRIC-A-knockout mice during young adulthood. These mutant mice showed significant hypertension and bradycardia. Autonomic blocking agents (co-application of atropine and metoprolol) greatly improved the bradycardic condition without affecting hypertension in the mutant mice. This observation suggests that a hyperactive baroreceptor reflex leads to development of the bradycardic condition in the mutant mice. Blockers for vasoactive humoral factors, such as angiotensin, endothelin and vasopressin, did not significantly improve hypertension in the mutant mice, suggesting normal blood-vasopressor levels. Importantly, isometric tension measurements indicated that contractility is markedly impaired in aortic ring preparations from the mutant mice, and that acetylcholine-induced relaxation is hypersensitive in mutant mesenteric artery. Our results suggest a vital role for TRIC-A channels in the physiological regulation of vessel tonus by vascular smooth muscle and endothelial cells. To further examine the pathogenesis of hypertension at the molecular level, we plan to examine TRIC-A expression and agonist-evoked Ca2+ transients in smooth muscle and endothelial cells from TRIC-A-knockout and wild-type mice." @default.
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- W2018892856 date "2010-01-01" @default.
- W2018892856 modified "2023-09-28" @default.
- W2018892856 title "Role of TRIC-A Channel in Circulatory Function" @default.
- W2018892856 doi "https://doi.org/10.1016/j.bpj.2009.12.3747" @default.
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