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10.1016/j.cardiores.2003.11.037 http://scihub22266oqcxt.onion/10.1016/j.cardiores.2003.11.037 14985063!ä!14985063 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 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\14985063.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cardiovasc+Res 2004 ; 61 (4): 663-70 Nephropedia Template TP {{tp|p=14985063|t=2004. Review of aldosterone- and angiotensin II-induced target organ damage and prevention |pdf=|usr=}}{{14985063}} gab.com Text Review of aldosterone- and angiotensin II-induced target organ damage and prevention JO: Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=14985063 #FOAvip Aldosterone is well recognized as a cause of sodium reabsorption, water retention, and potassium and magnesium loss; however, it also produces a variety of other actions that lead to progressive target organ damage in the heart, vasculature, and kidneys. Aldosterone interacts with mineralocorticoid receptors to promote endothelial dysfunction, facilitate thrombosis, reduce vascular compliance, impair baroreceptor function, and cause myocardial and vascular fibrosis. Although angiotensin II has been considered the major mediator of cardiovascular damage, increasing evidence suggests that aldosterone may mediate and exacerbate the damaging effects of angiotensin II. While angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers reduce plasma aldosterone levels initially, aldosterone rebound, or 'escape' may occur during long-term therapy. Therefore, aldosterone blockade is required to reduce the risk of progressive target organ damage in patients with hypertension and heart failure. This may be achieved nonselectively with spironolactone or with use of the selective aldosterone blocker eplerenone. While both agents have been demonstrated to be effective antihypertensive agents, eplerenone may produce improved target organ protection as witnessed in a variety of clinical settings, without the antiandrogenic and progestational effects commonly observed with spironolactone. Twit Text FOAVip Review of aldosterone- and angiotensin II-induced target organ damage and prevention ????Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=14985063 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=14985063 #FOAvip English Wikipedia <ref>{{Cite pmid|14985063}}</ref> Review of aldosterone- and angiotensin II-induced target organ damage and prevention #MMPMID14985063 Struthers AD; MacDonald TM Cardiovasc Res 2004[Mar]; 61 (4): 663-70 PMID14985063show ga Aldosterone is well recognized as a cause of sodium reabsorption, water retention, and potassium and magnesium loss; however, it also produces a variety of other actions that lead to progressive target organ damage in the heart, vasculature, and kidneys. Aldosterone interacts with mineralocorticoid receptors to promote endothelial dysfunction, facilitate thrombosis, reduce vascular compliance, impair baroreceptor function, and cause myocardial and vascular fibrosis. Although angiotensin II has been considered the major mediator of cardiovascular damage, increasing evidence suggests that aldosterone may mediate and exacerbate the damaging effects of angiotensin II. While angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers reduce plasma aldosterone levels initially, aldosterone rebound, or 'escape' may occur during long-term therapy. Therefore, aldosterone blockade is required to reduce the risk of progressive target organ damage in patients with hypertension and heart failure. This may be achieved nonselectively with spironolactone or with use of the selective aldosterone blocker eplerenone. While both agents have been demonstrated to be effective antihypertensive agents, eplerenone may produce improved target organ protection as witnessed in a variety of clinical settings, without the antiandrogenic and progestational effects commonly observed with spironolactone. |Aldosterone/*physiology[MESH] |Angiotensin II Type 2 Receptor Blockers[MESH] |Angiotensin II/*physiology[MESH] |Angiotensin-Converting Enzyme Inhibitors/therapeutic use[MESH] |Animals[MESH] |Cardiovascular Diseases/drug therapy/*metabolism[MESH] |Endothelium, Vascular/metabolism[MESH] |Eplerenone[MESH] |Humans[MESH] |Kidney/metabolism[MESH] |Mineralocorticoid Receptor Antagonists/therapeutic use[MESH] |Myocardium/*metabolism[MESH]Review of aldosterone- and angiotensin II-induced target organ damage (epmc).pdf DeepDyve Pubget Overpricing