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Inhibition of endoplasmic reticulum stress improves coronary artery function in the spontaneously hypertensive rats

 Soo-Kyoung Choi  ;  Mihwa Lim  ;  Seon-Hee Byeon  ;  Young-Ho Lee 
 SCIENTIFIC REPORTS, Vol.6 : 31925, 2016 
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Animals ; Biomarkers/metabolism ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Coronary Vessels/physiopathology* ; Disease Models, Animal ; Drug Administration Schedule ; Endoplasmic Reticulum Stress/drug effects* ; Gene Expression Regulation/drug effects ; Hypertension/drug therapy* ; Hypertension/metabolism ; Hypertension/physiopathology ; Male ; Phosphorylation/drug effects ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Taurochenodeoxycholic Acid/administration & dosage* ; Taurochenodeoxycholic Acid/pharmacology
Endoplasmic reticulum (ER) stress has been shown to play a critical role in the pathogenesis of cardiovascular complications. However, the role and mechanisms of ER stress in hypertension remain unclear. Thus, we hypothesized that enhanced ER stress contributes to the maintenance of hypertension in spontaneously hypertensive rats (SHRs). Sixteen-week old male SHRs and Wistar Kyoto Rats (WKYs) were used in this study. The SHRs were treated with ER stress inhibitor (Tauroursodeoxycholic acid; TUDCA, 100?mg/kg/day) for two weeks. There was a decrease in systolic blood pressure in SHR treated with TUDCA. The pressure-induced myogenic tone was significantly increased, whereas endothelium-dependent relaxation was significantly attenuated in SHR compared with WHY. Interestingly, treatment of ER stress inhibitor normalized myogenic responses and endothelium-dependent relaxation in SHR. These data were associated with an increase in expression or phosphorylation of ER stress markers (Bip, ATF6, CHOP, IRE1, XBP1, PERK, and eIF2α) in SHRs, which were reduced by TUDCA treatment. Furthermore, phosphorylation of MLC20 was increased in SHRs, which was reduced by the treatment of TUDCA. Therefore, our results suggest that ER stress could be a potential target for hypertension.
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1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Byeon, Seon Hee(변선희) ORCID logo https://orcid.org/0000-0001-9256-5209
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
Lim, Mi Hwa(임미화)
Choi, Soo Kyoung(최수경) ORCID logo https://orcid.org/0000-0002-7115-6358
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