Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.jpain.2014.04.005 http://scihub22266oqcxt.onion/10.1016/j.jpain.2014.04.005 C4264525!4264525!24793242     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Pain 2014 ; 15 (7): 771-7 Nephropedia Template TP {{tp|p=24793242|t=2014. ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia |pdf=|usr=}}{{24793242}} gab.com Text ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia JO: J Pain http://www.kidney.de/pget.php?&tw=1&pmid=24793242 #FOAvip Endothelin-1 acts on endothelial cells to enhance mechanical stimulation-induced release of ATP, which in turn can act on sensory neurons innervating blood vessels to contribute to vascular pain, a phenomenon we have referred to as stimulus-dependent hyperalgesia (SDH). In the present study we evaluated the role of the major classes of ATP release mechanisms to SDH: vesicular exocytosis, plasma membrane associated ATP synthase, ATP-Binding Cassette (ABC) transporters, and ion channels. Inhibitors of vesicular exocytosis (i.e., monensin, brefeldin A and bafilomycin), plasma membrane associated ATPase (i.e., oligomycin and pigment epithelium-derived factor-derived peptide 34-mer) and connexin ion channels (carbenoxolone and flufenamic acid), but not ABC transporters (i.e., dipyridamole, nicardipine or CFTRinh-172) attenuated stimulus-dependent hyperalgesia. These studies support a role of ATP in SDH, and suggest novel targets for the treatment of vascular pain syndromes. Twit Text FOAVip ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia ????J Pain http://www.kidney.de/pget.php?&tw=1&pmid=24793242 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24793242 #FOAvip English Wikipedia <ref>{{Cite pmid|24793242}}</ref> ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia #MMPMID24793242 Joseph EK; Green PG; Levine JD J Pain 2014[Jul]; 15 (7): 771-7 PMID24793242show ga Endothelin-1 acts on endothelial cells to enhance mechanical stimulation-induced release of ATP, which in turn can act on sensory neurons innervating blood vessels to contribute to vascular pain, a phenomenon we have referred to as stimulus-dependent hyperalgesia (SDH). In the present study we evaluated the role of the major classes of ATP release mechanisms to SDH: vesicular exocytosis, plasma membrane associated ATP synthase, ATP-Binding Cassette (ABC) transporters, and ion channels. Inhibitors of vesicular exocytosis (i.e., monensin, brefeldin A and bafilomycin), plasma membrane associated ATPase (i.e., oligomycin and pigment epithelium-derived factor-derived peptide 34-mer) and connexin ion channels (carbenoxolone and flufenamic acid), but not ABC transporters (i.e., dipyridamole, nicardipine or CFTRinh-172) attenuated stimulus-dependent hyperalgesia. These studies support a role of ATP in SDH, and suggest novel targets for the treatment of vascular pain syndromes. äATP release mechanisms of endothelial cell-mediated stimulus-dependent(epmc).pdf DeepDyve Pubget Overpricing