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Silencing of Atp2b1 increases blood pressure through vasoconstriction.

Title
Silencing of Atp2b1 increases blood pressure through vasoconstriction.
Authors
Young-Bin Shin;Ji Eun Lim;Bermseok Oh;Young-Ho Lee;Mark I. McCarthy;Mihwa Lim;Kyung-Won Hong;So-Yon Park;Hyeon-Ju Lee;Su-Min Ji
Issue Date
2013
Journal Title
Journal of Hypertension
ISSN
0263-6352
Citation
Journal of Hypertension, Vol.31(8) : 1575~1583, 2013
Abstract
BACKGROUND: Recent genome-wide association studies (GWASs) have identified 30 genetic loci that regulate blood pressure, increasing our understanding of the cause of hypertension. However, it has been difficult to define the causative genes at these loci due to a lack of functional analyses. METHOD: In this study, we aimed to validate the candidate gene ATP2B1 in 12q21, variants near which have the strongest association with blood pressure in Asians and Europeans. ATP2B1 functions as a calcium pump to fine-tune calcium concentrations - necessary for repolarization following muscular contractions. We silenced Atp2b1 using an siRNA complex, injected into mouse tail veins. RESULTS: In treated mice, blood pressure rose and the mesenteric arteries increased in wall : lumen ratio. Moreover, the arteries showed enhanced myogenic responses to pressure, and contractile responses to phenylephrine increased compared with the control, suggesting that blood pressure is regulated by ATP2B1 through the contraction and dilation of the vessel, likely by controlling calcium concentrations in the resting state. CONCLUSION: These results support that ATP2B1 is the causative gene in the blood pressure-associated 12q21 locus and demonstrate that ATP2B1 expression in the vessel influences blood pressure.
URI
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00004872-201308000-00014&LSLINK=80&D=ovft

http://ir.ymlib.yonsei.ac.kr/handle/22282913/87621
DOI
10.1097/HJH.0b013e32836189e9
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Physiology
Yonsei Authors
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