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Title: TRIC-A Channels in Vascular Smooth Muscle Contribute to Blood Pressure Maintenance.
Authors: Yamazaki, Daiju  KAKEN_id
Tabara, Yasuharu  kyouindb  KAKEN_id
Kita, Satomi
Hanada, Hironori
Komazaki, Shinji
Naitou, Daisuke
Mishima, Aya
Nishi, Miyuki  kyouindb  KAKEN_id
Yamamura, Hisao
Yamamoto, Shinichiro
Kakizawa, Sho  kyouindb  KAKEN_id
Miyachi, Hitoshi
Yamamoto, Shintaro
Miyata, Toshiyuki
Kawano, Yuhei
Kamide, Kei
Ogihara, Toshio
Hata, Akira
Umemura, Satoshi
Soma, Masayoshi
Takahashi, Norio
Imaizumi, Yuji
Miki, Tetsuro
Iwamoto, Takahiro
Takeshima, Hiroshi  kyouindb  KAKEN_id
Issue Date: 3-Aug-2011
Publisher: Elsevier
Citation: Yamazaki D, Tabara Y, Kita S, Hanada H, Komazaki S, Naitou D, Mishima A, Nishi M, Yamamura H, Yamamoto S, Kakizawa S, Miyachi H, Yamamoto S, Miyata T, Kawano Y, Kamide K, Ogihara T, Hata A, Umemura S, Soma M, Takahashi N, Imaizumi Y, Miki T, Iwamoto T, Takeshima H. TRIC-A Channels in Vascular Smooth Muscle Contribute to Blood Pressure Maintenance. Cell Metab. 2011 Aug 3;14(2):231-41.
Journal title: Cell metabolism
Volume: 14
Issue: 2
Start page: 231
End page: 241
Abstract: 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.
Description: 小胞体カウンターイオンチャネルTRICチャネルによる血圧調節機構とTRICチャネル遺伝子多型による本態性高血圧リスク. 京都大学プレスリリース. 2011-08-02.
Rights: © 2011 Elsevier Inc. All rights reserved.
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
URL: http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B7MFH-53FSRYK-H-1&_cdi=23259&_user=119230&_pii=S1550413111002178&_origin=gateway&_coverDate=08%2F03%2F2011&_sk=%23TOC%2323259%232011%23999859997%233458964%23FLA%23display%23Volume_14,_Issue_2,_Pages_143-280_%283_August_2011%29%23tagged%23Volume%23first%3D14%23Issue%23first%3D2%23date%23%283_August_2011%29%23&view=c&_gw=y&wchp=dGLzVzb-zSkWW&md5=9d6681ac09f2dd2e8a01f6d241047443&ie=/sdarticle.pdf
URI: http://hdl.handle.net/2433/143634
DOI(Published Version): 10.1016/j.cmet.2011.05.011
PubMed ID: 21803293
Related Link: http://www.kyoto-u.ac.jp/ja/news_data/h/h1/news6/2011/110802_1.htm
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