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Metformin prevents vascular damage in hypertension through the AMPK/ER stress pathway

Authors
 Cheng Chen  ;  Adam Kassan  ;  Diana Castañeda  ;  Mohanad Gabani  ;  Soo-Kyoung Choi  ;  Modar Kassan 
Citation
 HYPERTENSION RESEARCH, Vol.42(7) : 960-969, 2019 
Journal Title
 HYPERTENSION RESEARCH 
ISSN
 0916-9636 
Issue Date
2019
Keywords
AMP-activated protein kinase ; Angiotensin II ; Hypertension ; Metformin ; endoplasmic reticulum stress
Abstract
Metformin is an antidiabetic drug. However, the pleiotropic beneficial effects of metformin in nondiabetic models still need to be defined. The objective of this study is to investigate the effect of metformin on angiotensin II (Ang II)-induced hypertension and cardiovascular diseases. Mice were infused with Ang II (400 ng/kg per min) with or without metformin for 2 weeks. Mice infused with angiotensin II displayed an increase in blood pressure associated with enhanced vascular endoplasmic reticulum (ER) stress markers, which were blunted after metformin treatment. Moreover, hypertension-induced reduction in phosphorylated AMPK, endothelial nitric oxide synthase (eNOs) phosphorylation, and endothelium-dependent relaxation (EDR) in mesenteric resistance arteries (MRA) were rescued after metformin treatment. Infusion of ER stress inducer (tunicamycin, Tun) in control mice induced ER stress in MRA and reduced phosphorylation of AMPK, eNOS synthase phosphorylation, and EDR in MRA without affecting systolic blood pressure (SBP). All these factors were reversed subsequently with metformin treatment. ER stress inhibition by metformin improves vascular function in hypertension. Therefore, metformin could be a potential therapy for cardiovascular diseases in hypertension independent of its effects on diabetes.
Files in This Item:
T201904855.pdf Download
DOI
10.1038/s41440-019-0212-z
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Choi, Soo Kyoung(최수경) ORCID logo https://orcid.org/0000-0002-7115-6358
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/174544
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