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High fat diet confers vascular hyper-contractility against angiotensin II through upregulation of MLCK and CPI-17
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  • High fat diet confers vascular hyper-contractility against angiotensin II through upregulation of MLCK and CPI-17
저자명
JeeInKim
간행물명
The Korean Journal of Physiology & PharmacologyKCI,SCI,SCOPUS
권/호정보
2017년|21권 1호(통권121호)|pp.99-106 (8 pages)
발행정보
대한생리학회-대한약리학회|한국
파일정보
정기간행물|ENG|
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영문초록

Obesity is a critical risk factor for the hypertension. Although angiotensin II (Ang II) in obese individuals is known to be upregulated in obesity-induced hypertension, direct evidence that explains the underlying mechanism for increased vascular tone and consequent increase in blood pressure (BP) is largely unknown. The purpose of this study is to investigate the novel mechanism underlying Ang II-induced hyper-contractility and hypertension in obese rats. Eight-week old male Sprague-Dawley rats were fed with 60% fat diet or normal diet for 4 months. Body weight, plasma lipid profile, plasma Ang II level, BP, Ang II-induced vascular contraction, and expression of regulatory proteins modulating vascular contraction with/without Ang II stimulation were measured. As a result, high fat diet (HFD) accelerated age-dependent body weight gaining along with increased plasma Ang II concentration. It also increased BP and Ang II-induced aortic contraction. Basal expression of p-CPI-17 and myosin light chain (MLC) kinase was increased by HFD along with increased phosphorylation of MLC. Ang II-induced phosphorylation of CPI-17 and MLC were also higher in HFD group than control group. In conclusion HFD-induced hypertension is through at least in part by increased vascular contractility via increased expression and activation of contractile proteins and subsequent MLC phosphorylation induced by increased Ang II.

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