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10.3317/jraas.2003.024 http://scihub22266oqcxt.onion/10.3317/jraas.2003.024 14608519!ä!14608519 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\14608519.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Renin+Angiotensin+Aldosterone+Syst 2003 ; 4 (3): 155-63 Nephropedia Template TP {{tp|p=14608519|t=2003. Toward a broader understanding of aldosterone in congestive heart failure |pdf=|usr=}}{{14608519}} gab.com Text Toward a broader understanding of aldosterone in congestive heart failure JO: J Renin Angiotensin Aldosterone Syst http://www.kidney.de/pget.php?&tw=1&pmid=14608519 #FOAvip Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na+ resorption at the expense of K+ excretion in classic target tissues: kidneys, colon, sweat and salivary glands. Though less well known, Mg2+ excretion is likewise enhanced by ALDO, while adrenal ALDO secretion is regulated by extracellular Mg2+ ([Mg2+]o). An emerging body of information has and continues to identify other endocrine actions of ALDO receptor-ligand binding. They include: promoting an efflux of cytosolic free Mg2+, or [Mg2+]i, in exchange for Na+ in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na+ appetite, Na+ and H2O excretion and sympathetic nerve activity, and the regulation of TNF-alpha production from central and/or peripheral sources. Extra-adrenal steroidogenesis and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDOs contribution to the pathophysiology of congestive heart failure will undoubtedly emerge. Twit Text FOAVip Toward a broader understanding of aldosterone in congestive heart failure ????J Renin Angiotensin Aldosterone Syst http://www.kidney.de/pget.php?&tw=1&pmid=14608519 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=14608519 #FOAvip English Wikipedia <ref>{{Cite pmid|14608519}}</ref> Toward a broader understanding of aldosterone in congestive heart failure #MMPMID14608519 Weber KT; Sun Y; Wodi LA; Munir A; Jahangir E; Ahokas RA; Gerling IC; Postlethwaite AE; Warrington KJ J Renin Angiotensin Aldosterone Syst 2003[Sep]; 4 (3): 155-63 PMID14608519show ga Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na+ resorption at the expense of K+ excretion in classic target tissues: kidneys, colon, sweat and salivary glands. Though less well known, Mg2+ excretion is likewise enhanced by ALDO, while adrenal ALDO secretion is regulated by extracellular Mg2+ ([Mg2+]o). An emerging body of information has and continues to identify other endocrine actions of ALDO receptor-ligand binding. They include: promoting an efflux of cytosolic free Mg2+, or [Mg2+]i, in exchange for Na+ in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na+ appetite, Na+ and H2O excretion and sympathetic nerve activity, and the regulation of TNF-alpha production from central and/or peripheral sources. Extra-adrenal steroidogenesis and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDOs contribution to the pathophysiology of congestive heart failure will undoubtedly emerge. |Aldosterone/*physiology[MESH] |Animals[MESH] |Heart Failure/*physiopathology[MESH] |Humans[MESH]Toward a broader understanding of aldosterone in congestive heart fail(epmc).pdf DeepDyve Pubget Overpricing