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10.1016/s0002-9149(88)80016-x http://scihub22266oqcxt.onion/10.1016/s0002-9149(88)80016-x 3414540!ä!3414540 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       Am+J+Cardiol 1988 ; 62 (8): 72E-75E Nephropedia Template TP {{tp|p=3414540|t=1988. Control of renal perfusion and function in congestive heart failure |pdf=|usr=}}{{3414540}} gab.com Text Control of renal perfusion and function in congestive heart failure JO: Am J Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=3414540 #FOAvip The force that shaped the evolution of the kidney, anatomically and functionally, has been defense of extracellular fluid volume. Similarly, the role of the renin-angiotensin-aldosterone system in normal physiology involves volume homeostasis rather than blood pressure control. When a volume deficit occurs, e.g., by restriction of sodium intake or through hemorrhage, a substantial part of the renal vasoconstriction that occurs is due to angiotensin II. In this context, the renal response to congestive heart failure resembles the response to a volume deficit, with angiotensin-mediated renal vasoconstriction contributing to the decrease in blood flow, glomerular filtration rate and to sodium retention. Thus, converting-enzyme inhibition improves renal perfusion and function, including sodium, potassium, magnesium and water handling, as a major part of its therapeutic contribution in congestive heart failure. Twit Text FOAVip Control of renal perfusion and function in congestive heart failure ????Am J Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=3414540 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=3414540 #FOAvip English Wikipedia <ref>{{Cite pmid|3414540}}</ref> Control of renal perfusion and function in congestive heart failure #MMPMID3414540 Hollenberg NK Am J Cardiol 1988[Sep]; 62 (8): 72E-75E PMID3414540show ga The force that shaped the evolution of the kidney, anatomically and functionally, has been defense of extracellular fluid volume. Similarly, the role of the renin-angiotensin-aldosterone system in normal physiology involves volume homeostasis rather than blood pressure control. When a volume deficit occurs, e.g., by restriction of sodium intake or through hemorrhage, a substantial part of the renal vasoconstriction that occurs is due to angiotensin II. In this context, the renal response to congestive heart failure resembles the response to a volume deficit, with angiotensin-mediated renal vasoconstriction contributing to the decrease in blood flow, glomerular filtration rate and to sodium retention. Thus, converting-enzyme inhibition improves renal perfusion and function, including sodium, potassium, magnesium and water handling, as a major part of its therapeutic contribution in congestive heart failure. |*Renal Circulation[MESH] |Angiotensin-Converting Enzyme Inhibitors/therapeutic use[MESH] |Animals[MESH] |Blood Pressure[MESH] |Blood Volume[MESH] |Body Water/metabolism[MESH] |Glomerular Filtration Rate[MESH] |Heart Failure/drug therapy/metabolism/*physiopathology[MESH] |Humans[MESH] |Kidney/metabolism/*physiopathology[MESH] |Magnesium/metabolism[MESH] |Potassium/metabolism[MESH] |Sodium/metabolism[MESH]Control of renal perfusion and function in congestive heart failure (epmc).pdf DeepDyve Pubget Overpricing