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10.1113/JP276962 http://scihub22266oqcxt.onion/10.1113/JP276962 30307615!7496613!30307615     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       J+Physiol 2020 ; 598 (14): 2957-2976 Nephropedia Template TP {{tp|p=30307615|t=2020. Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches |pdf=|usr=}}{{30307615}} gab.com Text Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches JO: J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=30307615 #FOAvip Cardiac sympathetic overactivity is a well-established contributor to the progression of neurogenic hypertension and heart failure, yet the underlying pathophysiology remains unclear. Recent studies have highlighted the importance of acutely regulated cyclic nucleotides and their effectors in the control of intracellular calcium and exocytosis. Emerging evidence now suggests that a significant component of sympathetic overactivity and enhanced transmission may arise from impaired cyclic nucleotide signalling, resulting from compromised phosphodiesterase activity, as well as alterations in receptor-coupled G-protein activation. In this review, we address some of the key cellular and molecular pathways that contribute to sympathetic overactivity in hypertension and discuss their potential for therapeutic targeting. Twit Text FOAVip Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches ????J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=30307615 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30307615 #FOAvip English Wikipedia <ref>{{Cite pmid|30307615}}</ref> Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches #MMPMID30307615 Bardsley EN; Paterson DJ J Physiol 2020[Jul]; 598 (14): 2957-2976 PMID30307615show ga Cardiac sympathetic overactivity is a well-established contributor to the progression of neurogenic hypertension and heart failure, yet the underlying pathophysiology remains unclear. Recent studies have highlighted the importance of acutely regulated cyclic nucleotides and their effectors in the control of intracellular calcium and exocytosis. Emerging evidence now suggests that a significant component of sympathetic overactivity and enhanced transmission may arise from impaired cyclic nucleotide signalling, resulting from compromised phosphodiesterase activity, as well as alterations in receptor-coupled G-protein activation. In this review, we address some of the key cellular and molecular pathways that contribute to sympathetic overactivity in hypertension and discuss their potential for therapeutic targeting. |*Heart Failure[MESH] |*Hypertension/drug therapy[MESH] |Heart[MESH] |Humans[MESH]Neurocardiac regulation: from cardiac mechanisms to novel therapeutic (epmc).pdf DeepDyve Pubget Overpricing