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10.1111/bph.13833 http://scihub22266oqcxt.onion/10.1111/bph.13833 C5466537!5466537 !28436023     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28436023 &cmd=llinks): Failed to open stream: HTTP request failed! 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Activation of AMP-activated protein kinase by metformin ablates angiotensin II-induced endoplasmic reticulum stress and hypertension in mice in vivo |pdf=|usr=}}{{28436023 }} gab.com Text Activation of AMP-activated protein kinase by metformin ablates angiotensin II-induced endoplasmic reticulum stress and hypertension in mice in vivo JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=28436023 #FOAvip BACKGROUND AND PURPOSE: Metformin, one of the most frequently prescribed medications for type 2 diabetes, reportedly exerts BP-lowering effects in patients with diabetes. However, the effects and underlying mechanisms of metformin on BP in non-diabetic conditions remain to be determined. The aim of the present study was to determine the effects of metformin on angiotensin II (Ang II) infusion-induced hypertension in vivo. EXPERIMENTAL APPROACH: The effects of metformin on BP were investigated in wild-type (WT) C57BL/6J mice and in mice lacking AMP-activated protein kinase ?2 (AMPK?2) mice with or without Ang II infusion. Also, the effect of metformin on Ang II-induced endoplasmic reticulum (ER) stress was explored in cultured human vascular smooth muscle cells (hVSMCs). KEY RESULTS: Metformin markedly reduced BP in Ang II-infused WT mice but not in AMPK?2-deficient mice. In cultured hVSMCs, Ang II treatment resulted in inactivation of AMPK, as well as the subsequent induction of spliced X-box binding protein-1, phosphorylation of eukaryotic translation initiation factor 2? and expression of glucose-regulated protein 78 kDa, representing three well-characterized ER stress biomarkers. Moreover, AMPK activation by metformin ablated Ang II-induced ER stress in hVSMCs. Mechanistically, metformin-activated AMPK?2 suppressed ER stress by increasing phospholamban phosphorylation. CONCLUSION AND IMPLICATIONS: Metformin alleviates Ang II-triggered hypertension in mice by activating AMPK?2, which mediates phospholamban phosphorylation and inhibits Ang II-induced ER stress in vascular smooth muscle cells. Twit Text FOAVip Activation of AMP-activated protein kinase by metformin ablates angiotensin II-induced endoplasmic reticulum stress and hypertension in mice in vivo ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=28436023 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28436023 #FOAvip English Wikipedia <ref>{{Cite pmid|28436023 }}</ref> Activation of AMP-activated protein kinase by metformin ablates angiotensin II-induced endoplasmic reticulum stress and hypertension in mice in vivo #MMPMID28436023 Duan Q ; Song P ; Ding Y ; Zou MH Br J Pharmacol 2017[Jul]; 174 (13 ): 2140-2151 PMID28436023 show ga BACKGROUND AND PURPOSE: Metformin, one of the most frequently prescribed medications for type 2 diabetes, reportedly exerts BP-lowering effects in patients with diabetes. However, the effects and underlying mechanisms of metformin on BP in non-diabetic conditions remain to be determined. The aim of the present study was to determine the effects of metformin on angiotensin II (Ang II) infusion-induced hypertension in vivo. EXPERIMENTAL APPROACH: The effects of metformin on BP were investigated in wild-type (WT) C57BL/6J mice and in mice lacking AMP-activated protein kinase ?2 (AMPK?2) mice with or without Ang II infusion. Also, the effect of metformin on Ang II-induced endoplasmic reticulum (ER) stress was explored in cultured human vascular smooth muscle cells (hVSMCs). KEY RESULTS: Metformin markedly reduced BP in Ang II-infused WT mice but not in AMPK?2-deficient mice. In cultured hVSMCs, Ang II treatment resulted in inactivation of AMPK, as well as the subsequent induction of spliced X-box binding protein-1, phosphorylation of eukaryotic translation initiation factor 2? and expression of glucose-regulated protein 78 kDa, representing three well-characterized ER stress biomarkers. Moreover, AMPK activation by metformin ablated Ang II-induced ER stress in hVSMCs. Mechanistically, metformin-activated AMPK?2 suppressed ER stress by increasing phospholamban phosphorylation. CONCLUSION AND IMPLICATIONS: Metformin alleviates Ang II-triggered hypertension in mice by activating AMPK?2, which mediates phospholamban phosphorylation and inhibits Ang II-induced ER stress in vascular smooth muscle cells. |AMP-Activated Protein Kinases/deficiency/*metabolism [MESH] |Angiotensin II/*drug effects/metabolism [MESH] |Animals [MESH] |Cells, Cultured [MESH] |Dose-Response Relationship, Drug [MESH] |Endoplasmic Reticulum Stress/*drug effects [MESH] |Humans [MESH] |Hypertension/*drug therapy/metabolism [MESH] |Metformin/administration & dosage/*pharmacology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Muscle, Smooth, Vascular/drug effects/metabolism [MESH]Activation of AMP-activated protein kinase by metformin ablates angiot(epmc).pdf DeepDyve Pubget Overpricing