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10.1053/j.ackd.2014.12.005 http://scihub22266oqcxt.onion/10.1053/j.ackd.2014.12.005 C4410676!4410676!25908473     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 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       Adv+Chronic+Kidney+Dis 2015 ; 22 (3): 232-44 Nephropedia Template TP {{tp|p=25908473|t=2015. ENDOGENOUS CARDIOTONIC STEROIDS IN KIDNEY FAILURE: A REVIEW AND A HYPOTHESIS |pdf=|usr=}}{{25908473}} gab.com Text ENDOGENOUS CARDIOTONIC STEROIDS IN KIDNEY FAILURE: A REVIEW AND A HYPOTHESIS JO: Adv Chronic Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=25908473 #FOAvip In response to progressive nephron loss, volume and humoral signals in the circulation have increasing relevance. These signals, including plasma sodium, angiotensin II and those related to volume status, activate a slow neuromodulatory pathway within the central nervous system (CNS). The slow CNS pathway includes specific receptors for angiotensin II, mineralocorticoids, and endogenous ouabain (EO). Stimulation of the pathway leads to elevated sympathetic nervous system activity (SNA) and increased circulating EO. The sustained elevation of circulating EO (or ouabain) stimulates central and peripheral mechanisms that amplify the impact of SNA on vascular tone. These include: changes in synaptic plasticity in the brain and sympathetic ganglia that increase preganglionic tone and amplify ganglionic transmission, amplification of the impact of SNA on arterial tone in the vascular wall, and the reprogramming of calcium signaling proteins in arterial myocytes. These increase SNA, raise basal and evoked arterial tone, and elevate blood pressure (BP). In the setting of chronic kidney disease, we suggest that sustained elevation of the slow CNS pathway, plasma EO and the cardiotonic steroid marinobufagenin (MBG), comprise a feed-forward system that raises BP and accelerates kidney and cardiac damage. Block of the slow CNS pathway and/or circulating EO and MBG may reduce BP and slow the progression to end stage renal disease. Twit Text FOAVip ENDOGENOUS CARDIOTONIC STEROIDS IN KIDNEY FAILURE: A REVIEW AND A HYPOTHESIS ????Adv Chronic Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=25908473 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25908473 #FOAvip English Wikipedia <ref>{{Cite pmid|25908473}}</ref> ENDOGENOUS CARDIOTONIC STEROIDS IN KIDNEY FAILURE: A REVIEW AND A HYPOTHESIS #MMPMID25908473 Hamlyn JM; Manunta P Adv Chronic Kidney Dis 2015[May]; 22 (3): 232-44 PMID25908473show ga In response to progressive nephron loss, volume and humoral signals in the circulation have increasing relevance. These signals, including plasma sodium, angiotensin II and those related to volume status, activate a slow neuromodulatory pathway within the central nervous system (CNS). The slow CNS pathway includes specific receptors for angiotensin II, mineralocorticoids, and endogenous ouabain (EO). Stimulation of the pathway leads to elevated sympathetic nervous system activity (SNA) and increased circulating EO. The sustained elevation of circulating EO (or ouabain) stimulates central and peripheral mechanisms that amplify the impact of SNA on vascular tone. These include: changes in synaptic plasticity in the brain and sympathetic ganglia that increase preganglionic tone and amplify ganglionic transmission, amplification of the impact of SNA on arterial tone in the vascular wall, and the reprogramming of calcium signaling proteins in arterial myocytes. These increase SNA, raise basal and evoked arterial tone, and elevate blood pressure (BP). In the setting of chronic kidney disease, we suggest that sustained elevation of the slow CNS pathway, plasma EO and the cardiotonic steroid marinobufagenin (MBG), comprise a feed-forward system that raises BP and accelerates kidney and cardiac damage. Block of the slow CNS pathway and/or circulating EO and MBG may reduce BP and slow the progression to end stage renal disease. äENDOGENOUS CARDIOTONIC STEROIDS IN KIDNEY FAILURE: A REVIEW AND A HYPO(epmc).pdf DeepDyve Pubget Overpricing