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10.1007/s00210-009-0464-2 http://scihub22266oqcxt.onion/10.1007/s00210-009-0464-2 19894037!ä!19894037 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Naunyn+Schmiedebergs+Arch+Pharmacol 2009 ; 380 (6): 497-507 Nephropedia Template TP {{tp|p=19894037|t=2009. Inhibitors of TRP channels reveal stimulus-dependent differential activation of Ca2+ influx pathways in human neutrophil granulocytes |pdf=|usr=}}{{19894037}} gab.com Text Inhibitors of TRP channels reveal stimulus-dependent differential activation of Ca2+ influx pathways in human neutrophil granulocytes JO: Naunyn Schmiedebergs Arch Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=19894037 #FOAvip A pharmacological characterization of Ca(2+) influx pathways in neutrophil granulocytes is problematic because of the lack of specific inhibitors. The activation of transient receptor potential cation channel, subfamily M, member 2 (TRPM2) channels by intracellular adenosine diphosphate ribose (ADPR), well characterized in neutrophils, is reportedly inhibited by 8-bromo-ADPR (8Br-ADPR). TRPM2 is blocked by N-(p-amylcinnamoyl)anthranilic acid (ACA) interfering with the pore, but ACA is as well effective on other transient receptor potential channels, especially transient receptor potential canonical (TRPC) channels. We wished to analyze whether ACA and 8Br-ADPR were suitable probes to demonstrate that different Ca(2+) entry pathways are activated in human neutrophil granulocytes by the receptor-dependent stimuli N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) and platelet-activating factor (PAF) and the receptor-independent thapsigargin. Ca(2+)-influx-related increases in [Ca(2+)](i) were calculated by comparing aliquots of fluo-3-loaded neutrophils in the presence and absence of extracellular Ca(2+). Moreover, Mn(2+) quenching was used in fura-2-loaded cells. We compared 8Br-ADPR with ACA. 8Br-ADPR was exclusively effective when Ca(2+) influx (or Mn(2+) quenching) was induced by fMLP; it did not affect influx when PAF or thapsigargin was the stimulus. ACA inhibited Ca(2+) influx significantly more strongly when this was induced by PAF than by fMLP. Moreover, it reduced thapsigargin-induced Ca(2+) influx. The contribution of TRPM2 to Ca(2+) influx in neutrophils strongly depends on the stimulus; it is sizeable in the case of fMLP and minimal in the case of PAF. PAF induces Ca(2+) entry pathways different from TRPM2; the inhibition by ACA suggests the contribution of channels of the TRPC family. Twit Text FOAVip Inhibitors of TRP channels reveal stimulus-dependent differential activation of Ca2+ influx pathways in human neutrophil granulocytes ????Naunyn Schmiedebergs Arch Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=19894037 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19894037 #FOAvip English Wikipedia <ref>{{Cite pmid|19894037}}</ref> Inhibitors of TRP channels reveal stimulus-dependent differential activation of Ca2+ influx pathways in human neutrophil granulocytes #MMPMID19894037 Pantaler E; Luckhoff A Naunyn Schmiedebergs Arch Pharmacol 2009[Dec]; 380 (6): 497-507 PMID19894037show ga A pharmacological characterization of Ca(2+) influx pathways in neutrophil granulocytes is problematic because of the lack of specific inhibitors. The activation of transient receptor potential cation channel, subfamily M, member 2 (TRPM2) channels by intracellular adenosine diphosphate ribose (ADPR), well characterized in neutrophils, is reportedly inhibited by 8-bromo-ADPR (8Br-ADPR). TRPM2 is blocked by N-(p-amylcinnamoyl)anthranilic acid (ACA) interfering with the pore, but ACA is as well effective on other transient receptor potential channels, especially transient receptor potential canonical (TRPC) channels. We wished to analyze whether ACA and 8Br-ADPR were suitable probes to demonstrate that different Ca(2+) entry pathways are activated in human neutrophil granulocytes by the receptor-dependent stimuli N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) and platelet-activating factor (PAF) and the receptor-independent thapsigargin. Ca(2+)-influx-related increases in [Ca(2+)](i) were calculated by comparing aliquots of fluo-3-loaded neutrophils in the presence and absence of extracellular Ca(2+). Moreover, Mn(2+) quenching was used in fura-2-loaded cells. We compared 8Br-ADPR with ACA. 8Br-ADPR was exclusively effective when Ca(2+) influx (or Mn(2+) quenching) was induced by fMLP; it did not affect influx when PAF or thapsigargin was the stimulus. ACA inhibited Ca(2+) influx significantly more strongly when this was induced by PAF than by fMLP. Moreover, it reduced thapsigargin-induced Ca(2+) influx. The contribution of TRPM2 to Ca(2+) influx in neutrophils strongly depends on the stimulus; it is sizeable in the case of fMLP and minimal in the case of PAF. PAF induces Ca(2+) entry pathways different from TRPM2; the inhibition by ACA suggests the contribution of channels of the TRPC family. |Adenosine Diphosphate Ribose/*analogs & derivatives/pharmacology[MESH] |Aniline Compounds/chemistry[MESH] |Calcium/*metabolism[MESH] |Cinnamates/*pharmacology[MESH] |Fluorescent Dyes/chemistry[MESH] |Humans[MESH] |Manganese/chemistry[MESH] |N-Formylmethionine Leucyl-Phenylalanine/pharmacology[MESH] |Neutrophils/drug effects/metabolism[MESH] |Platelet Activating Factor/pharmacology[MESH] |TRPM Cation Channels/*antagonists & inhibitors/metabolism[MESH] |Thapsigargin/pharmacology[MESH] |Xanthenes/chemistry[MESH]Inhibitors of TRP channels reveal stimulus-dependent differential acti(epmc).pdf DeepDyve Pubget Overpricing