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10.1097/MNH.0000000000000306 http://scihub22266oqcxt.onion/10.1097/MNH.0000000000000306 C5382958!5382958!27930384     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Opin+Nephrol+Hypertens 2017 ; 26 (2): 97-104 Nephropedia Template TP {{tp|p=27930384|t=2017. The Endothelial Mineralocorticoid Receptor: Mediator of the Switch from Vascular Health to Disease |pdf=|usr=}}{{27930384}} gab.com Text The Endothelial Mineralocorticoid Receptor: Mediator of the Switch from Vascular Health to Disease JO: Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=27930384 #FOAvip Purpose of review: Endothelial dysfunction is an early feature of vascular disease induced by cardiovascular risk factors (CRF). In growing populations with obesity, diabetes, hypertension and heart failure, mineralocorticoid receptor (MR) antagonism improves endothelial function. This review summarizes recent advances in our understanding of the specific role of endothelial cell (EC) MR in vascular function in health and disease. Recent findings: Using transgenic mice with MR expression specifically modulated in ECs, recent studies support the emerging concept that while EC-MR may be protective in health, in the presence of CRFs, EC-MR contributes to endothelial dysfunction and progression of vascular disease. Proposed mechanisms include a role for EC-MR in decreased nitric oxide production and bioavailability, increased vascular oxidative stress, regulation of epithelial sodium channels that enhance vascular stiffness, and increased EC adhesion molecules promoting inflammation. The role of EC-MR may also depend on the sex, race, or vascular bed involved. Summary: Recent advances support the idea that EC-MR is a mediator of the switch from vascular health to disease in response to CRFs. Further investigation of the molecular mechanism is underway to identify therapeutic interventions that will limit the detrimental effects of EC-MR in patients at cardiovascular risk. Twit Text FOAVip The Endothelial Mineralocorticoid Receptor: Mediator of the Switch from Vascular Health to Disease ????Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=27930384 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27930384 #FOAvip English Wikipedia <ref>{{Cite pmid|27930384}}</ref> The Endothelial Mineralocorticoid Receptor: Mediator of the Switch from Vascular Health to Disease #MMPMID27930384 Davel A; Anwar I; Jaffe I Curr Opin Nephrol Hypertens 2017[Mar]; 26 (2): 97-104 PMID27930384show ga Purpose of review: Endothelial dysfunction is an early feature of vascular disease induced by cardiovascular risk factors (CRF). In growing populations with obesity, diabetes, hypertension and heart failure, mineralocorticoid receptor (MR) antagonism improves endothelial function. This review summarizes recent advances in our understanding of the specific role of endothelial cell (EC) MR in vascular function in health and disease. Recent findings: Using transgenic mice with MR expression specifically modulated in ECs, recent studies support the emerging concept that while EC-MR may be protective in health, in the presence of CRFs, EC-MR contributes to endothelial dysfunction and progression of vascular disease. Proposed mechanisms include a role for EC-MR in decreased nitric oxide production and bioavailability, increased vascular oxidative stress, regulation of epithelial sodium channels that enhance vascular stiffness, and increased EC adhesion molecules promoting inflammation. The role of EC-MR may also depend on the sex, race, or vascular bed involved. Summary: Recent advances support the idea that EC-MR is a mediator of the switch from vascular health to disease in response to CRFs. Further investigation of the molecular mechanism is underway to identify therapeutic interventions that will limit the detrimental effects of EC-MR in patients at cardiovascular risk. äThe Endothelial Mineralocorticoid Receptor: Mediator of the Switch fro(epmc).pdf DeepDyve Pubget Overpricing