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10.1016/j.ando.2020.04.005 http://scihub22266oqcxt.onion/10.1016/j.ando.2020.04.005 32370986!7172808!32370986     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+Endocrinol+(Paris) 2020 ; 81 (2-3): 63-67 Nephropedia Template TP {{tp|p=32370986|t=2020. Renin-angiotensin-aldosterone system and COVID-19 infection |pdf=|usr=}}{{32370986}} gab.com Text Renin-angiotensin-aldosterone system and COVID-19 infection JO: Ann Endocrinol (Paris) http://www.kidney.de/pget.php?&tw=1&pmid=32370986 #FOAvip With the multiplication of COVID-19 severe acute respiratory syndrome cases due to SARS-COV2, some concerns about angiotensin-converting enzyme 1 (ACE1) inhibitors (ACEi) and angiotensin II type 1 receptor blockers (ARB) have emerged. Since the ACE2 (angiotensin-converting enzyme 2) enzyme is the receptor that allows SARS COV2 entry into cells, the fear was that pre-existing treatment with ACEi or ARB might increase the risk of developing severe or fatal severe acute respiratory syndrome in case of COVID-19 infection. The present article discusses these concerns. ACE2 is a membrane-bound enzyme (carboxypeptidase) that contributes to the inactivation of angiotensin II and therefore physiologically counters angiotensin II effects. ACEis do not inhibit ACE2. Although ARBs have been shown to up-regulate ACE2 tissue expression in experimental animals, evidence was not always consistent in human studies. Moreover, to date there is no evidence that ACEi or ARB administration facilitates SARS-COV2 cell entry by increasing ACE2 tissue expression in either animal or human studies. Finally, some studies support the hypothesis that elevated ACE2 membrane expression and tissue activity by administration of ARB and/or infusion of soluble ACE2 could confer protective properties against inflammatory tissue damage in COVID-19 infection. In summary, based on the currently available evidence and as advocated by many medical societies, ACEi or ARB should not be discontinued because of concerns with COVID-19 infection, except when the hemodynamic situation is precarious and case-by-case adjustment is required. Twit Text FOAVip Renin-angiotensin-aldosterone system and COVID-19 infection ????Ann Endocrinol (Paris) http://www.kidney.de/pget.php?&tw=1&pmid=32370986 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32370986 #FOAvip English Wikipedia <ref>{{Cite pmid|32370986}}</ref> Renin-angiotensin-aldosterone system and COVID-19 infection #MMPMID32370986 Alexandre J; Cracowski JL; Richard V; Bouhanick B Ann Endocrinol (Paris) 2020[Jun]; 81 (2-3): 63-67 PMID32370986show ga With the multiplication of COVID-19 severe acute respiratory syndrome cases due to SARS-COV2, some concerns about angiotensin-converting enzyme 1 (ACE1) inhibitors (ACEi) and angiotensin II type 1 receptor blockers (ARB) have emerged. Since the ACE2 (angiotensin-converting enzyme 2) enzyme is the receptor that allows SARS COV2 entry into cells, the fear was that pre-existing treatment with ACEi or ARB might increase the risk of developing severe or fatal severe acute respiratory syndrome in case of COVID-19 infection. The present article discusses these concerns. ACE2 is a membrane-bound enzyme (carboxypeptidase) that contributes to the inactivation of angiotensin II and therefore physiologically counters angiotensin II effects. ACEis do not inhibit ACE2. Although ARBs have been shown to up-regulate ACE2 tissue expression in experimental animals, evidence was not always consistent in human studies. Moreover, to date there is no evidence that ACEi or ARB administration facilitates SARS-COV2 cell entry by increasing ACE2 tissue expression in either animal or human studies. Finally, some studies support the hypothesis that elevated ACE2 membrane expression and tissue activity by administration of ARB and/or infusion of soluble ACE2 could confer protective properties against inflammatory tissue damage in COVID-19 infection. In summary, based on the currently available evidence and as advocated by many medical societies, ACEi or ARB should not be discontinued because of concerns with COVID-19 infection, except when the hemodynamic situation is precarious and case-by-case adjustment is required. |Aldosterone/metabolism/*physiology[MESH] |Angiotensin II Type 1 Receptor Blockers/*therapeutic use[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Angiotensin-Converting Enzyme Inhibitors/*therapeutic use[MESH] |Betacoronavirus/*metabolism[MESH] |Blood Pressure/physiology[MESH] |COVID-19[MESH] |Comorbidity[MESH] |Coronavirus Infections/epidemiology/pathology/*physiopathology[MESH] |Humans[MESH] |Hypertension/drug therapy/epidemiology/physiopathology[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/*metabolism[MESH] |Pneumonia, Viral/epidemiology/pathology/*physiopathology[MESH] |Practice Guidelines as Topic[MESH] |Renin-Angiotensin System/*physiology[MESH] |SARS-CoV-2[MESH] |Severity of Illness Index[MESH]Renin-angiotensin-aldosterone system and COVID-19 infection (epmc).pdf DeepDyve Pubget Overpricing