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10.1152/ajpregu.00078.2015 http://scihub22266oqcxt.onion/10.1152/ajpregu.00078.2015 C4591381!4591381!26084692     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       Am+J+Physiol+Regul+Integr+Comp+Physiol 2015 ; 309 (5): R444-58 Nephropedia Template TP {{tp|p=26084692|t=2015. Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control |pdf=|usr=}}{{26084692}} gab.com Text Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26084692 #FOAvip Despite tremendous research efforts, hypertension remains an epidemic health concern, leading often to the development of cardiovascular disease. It is well established that in many instances, the brain plays an important role in the onset and progression of hypertension via activation of the sympathetic nervous system. Further, the activity of the renin-angiotensin system (RAS) and of glial cell-mediated proinflammatory processes have independently been linked to this neural control and are, as a consequence, both attractive targets for the development of antihypertensive therapeutics. Although it is clear that the predominant effector peptide of the RAS, ANG II, activates its type-1 receptor on neurons to mediate some of its hypertensive actions, additional nuances of this brain RAS control of blood pressure are constantly being uncovered. One of these complexities is that the RAS is now thought to impact cardiovascular control, in part, via facilitating a glial cell-dependent proinflammatory milieu within cardiovascular control centers. Another complexity is that the newly characterized antihypertensive limbs of the RAS are now recognized to, in many cases, antagonize the prohypertensive ANG II type 1 receptor (AT1R)-mediated effects. That being said, the mechanism by which the RAS, glia, and neurons interact to regulate blood pressure is an active area of ongoing research. Here, we review the current understanding of these interactions and present a hypothetical model of how these exchanges may ultimately regulate cardiovascular function. Twit Text FOAVip Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26084692 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26084692 #FOAvip English Wikipedia <ref>{{Cite pmid|26084692}}</ref> Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control #MMPMID26084692 de Kloet AD; Liu M; Rodríguez V; Krause EG; Sumners C Am J Physiol Regul Integr Comp Physiol 2015[Sep]; 309 (5): R444-58 PMID26084692show ga Despite tremendous research efforts, hypertension remains an epidemic health concern, leading often to the development of cardiovascular disease. It is well established that in many instances, the brain plays an important role in the onset and progression of hypertension via activation of the sympathetic nervous system. Further, the activity of the renin-angiotensin system (RAS) and of glial cell-mediated proinflammatory processes have independently been linked to this neural control and are, as a consequence, both attractive targets for the development of antihypertensive therapeutics. Although it is clear that the predominant effector peptide of the RAS, ANG II, activates its type-1 receptor on neurons to mediate some of its hypertensive actions, additional nuances of this brain RAS control of blood pressure are constantly being uncovered. One of these complexities is that the RAS is now thought to impact cardiovascular control, in part, via facilitating a glial cell-dependent proinflammatory milieu within cardiovascular control centers. Another complexity is that the newly characterized antihypertensive limbs of the RAS are now recognized to, in many cases, antagonize the prohypertensive ANG II type 1 receptor (AT1R)-mediated effects. That being said, the mechanism by which the RAS, glia, and neurons interact to regulate blood pressure is an active area of ongoing research. Here, we review the current understanding of these interactions and present a hypothetical model of how these exchanges may ultimately regulate cardiovascular function. äRole of neurons and glia in the CNS actions of the renin-angiotensin s(epmc).pdf DeepDyve Pubget Overpricing