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10.1152/ajpregu.00366.2014 http://scihub22266oqcxt.onion/10.1152/ajpregu.00366.2014 C4346759!4346759 !25519733     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25519733 &cmd=llinks): Failed to open stream: HTTP request failed! 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Brain ACE2 overexpression reduces DOCA-salt hypertension independently of endoplasmic reticulum stress |pdf=|usr=}}{{25519733 }} gab.com Text Brain ACE2 overexpression reduces DOCA-salt hypertension independently of endoplasmic reticulum stress JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25519733 #FOAvip Endoplasmic reticulum (ER) stress was previously reported to contribute to neurogenic hypertension while neuronal angiotensin-converting enzyme type 2 (ACE2) overexpression blunts the disease. To assess which brain regions are important for ACE2 beneficial effects and the contribution of ER stress to neurogenic hypertension, we first used transgenic mice harboring a floxed neuronal hACE2 transgene (SL) and tested the impact of hACE2 knockdown in the subfornical organ (SFO) and paraventricular nucleus (PVN) on deoxycorticosterone acetate (DOCA)-salt hypertension. SL and nontransgenic (NT) mice underwent DOCA-salt or sham treatment while infected with an adenoassociated virus (AAV) encoding Cre recombinase (AAV-Cre) or a control virus (AAV-green fluorescent protein) to the SFO or PVN. DOCA-salt-induced hypertension was reduced in SL mice, with hACE2 overexpression in the brain. This reduction was only partially blunted by knockdown of hACE2 in the SFO or PVN, suggesting that both regions are involved but not essential for ACE2 regulation of blood pressure (BP). DOCA-salt treatment did not increase the protein levels of ER stress and autophagy markers in NT mice, despite a significant increase in BP. In addition, these markers were not affected by hACE2 overexpression in the brain, despite a significant reduction of hypertension in SL mice. To further assess the role of ER stress in neurogenic hypertension, NT mice were infused intracerebroventricularlly with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor, during DOCA-salt treatment. However, TUDCA infusion failed to blunt the development of hypertension in NT mice. Our data suggest that brain ER stress does not contribute to DOCA-salt hypertension and that ACE2 blunts neurogenic hypertension independently of ER stress. Twit Text FOAVip Brain ACE2 overexpression reduces DOCA-salt hypertension independently of endoplasmic reticulum stress ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25519733 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25519733 #FOAvip English Wikipedia <ref>{{Cite pmid|25519733 }}</ref> Brain ACE2 overexpression reduces DOCA-salt hypertension independently of endoplasmic reticulum stress #MMPMID25519733 Xia H ; de Queiroz TM ; Sriramula S ; Feng Y ; Johnson T ; Mungrue IN ; Lazartigues E Am J Physiol Regul Integr Comp Physiol 2015[Mar]; 308 (5 ): R370-8 PMID25519733 show ga Endoplasmic reticulum (ER) stress was previously reported to contribute to neurogenic hypertension while neuronal angiotensin-converting enzyme type 2 (ACE2) overexpression blunts the disease. To assess which brain regions are important for ACE2 beneficial effects and the contribution of ER stress to neurogenic hypertension, we first used transgenic mice harboring a floxed neuronal hACE2 transgene (SL) and tested the impact of hACE2 knockdown in the subfornical organ (SFO) and paraventricular nucleus (PVN) on deoxycorticosterone acetate (DOCA)-salt hypertension. SL and nontransgenic (NT) mice underwent DOCA-salt or sham treatment while infected with an adenoassociated virus (AAV) encoding Cre recombinase (AAV-Cre) or a control virus (AAV-green fluorescent protein) to the SFO or PVN. DOCA-salt-induced hypertension was reduced in SL mice, with hACE2 overexpression in the brain. This reduction was only partially blunted by knockdown of hACE2 in the SFO or PVN, suggesting that both regions are involved but not essential for ACE2 regulation of blood pressure (BP). DOCA-salt treatment did not increase the protein levels of ER stress and autophagy markers in NT mice, despite a significant increase in BP. In addition, these markers were not affected by hACE2 overexpression in the brain, despite a significant reduction of hypertension in SL mice. To further assess the role of ER stress in neurogenic hypertension, NT mice were infused intracerebroventricularlly with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor, during DOCA-salt treatment. However, TUDCA infusion failed to blunt the development of hypertension in NT mice. Our data suggest that brain ER stress does not contribute to DOCA-salt hypertension and that ACE2 blunts neurogenic hypertension independently of ER stress. |*Desoxycorticosterone Acetate [MESH] |*Endoplasmic Reticulum Stress/drug effects [MESH] |*Sodium Chloride, Dietary [MESH] |Angiotensin-Converting Enzyme 2 [MESH] |Animals [MESH] |Biomarkers/metabolism [MESH] |Blood Pressure [MESH] |Brain/drug effects/*enzymology/physiopathology [MESH] |Disease Models, Animal [MESH] |Endoplasmic Reticulum/drug effects/*enzymology [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Hypertension/enzymology/genetics/physiopathology/*prevention & control [MESH] |Infusions, Intraventricular [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Paraventricular Hypothalamic Nucleus/enzymology/physiopathology [MESH] |Peptidyl-Dipeptidase A/genetics/*metabolism [MESH] |Subfornical Organ/enzymology/physiopathology [MESH] |Taurochenodeoxycholic Acid/administration & dosage [MESH] |Time Factors [MESH]Brain ACE2 overexpression reduces DOCA-salt hypertension independently(epmc).pdf DeepDyve Pubget Overpricing