{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:45:56Z","timestamp":1787013956777,"version":"build-2736575974"},"reference-count":62,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,5,27]],"date-time":"2013-05-27T00:00:00Z","timestamp":1369612800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2013,6]]},"abstract":"\n Background and Purpose<\/jats:title>\n \n N<\/jats:styled-content>\n \u2010arachidonoyl glycine (\n NAGly<\/jats:styled-content>\n ) is a lipoamino acid with vasorelaxant properties. We aimed to explore the mechanisms of\n NAGly's<\/jats:styled-content>\n action on unstimulated and agonist\u2010stimulated endothelial cells.\n <\/jats:p>\n <\/jats:sec>\n \n Experimental Approach<\/jats:title>\n \n The effects of\n NAGly<\/jats:styled-content>\n on endothelial electrical signalling were studied in combination with vascular reactivity.\n <\/jats:p>\n <\/jats:sec>\n \n Key Results<\/jats:title>\n \n I<\/jats:styled-content>\n n\n EA<\/jats:styled-content>\n .hy926 cells, the sustained hyperpolarization to histamine was inhibited by the non\u2010selective\n \n \n Na\n +<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n \/\n \n \n Ca\n 2+<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n exchanger (\n NCX<\/jats:styled-content>\n ) inhibitor bepridil and by an inhibitor of reversed mode\n NCX, KB<\/jats:styled-content>\n \u2010R7943. In cells dialysed with\n \n \n Cs\n +<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n \u2010based\n \n \n Na\n +<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n \u2010containing solution, the outwardly rectifying current with typical characteristics of\n NCX<\/jats:styled-content>\n was augmented following histamine exposure, further increased upon external\n \n \n Na\n +<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n withdrawal and inhibited by bepridil.\n NAGly<\/jats:styled-content>\n (0.3\u201330\u2009\u03bcM) suppressed\n NCX<\/jats:styled-content>\n currents in a\n URB597<\/jats:styled-content>\n \u2010 and guanosine 5\u2032\u2010O\u2010(2\u2010thiodiphosphate) (\n GDP<\/jats:styled-content>\n \u03b2\n S<\/jats:styled-content>\n )\u2010insensitive manner, [\n \n \n Ca\n 2+<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n ]\n i<\/jats:sub>\n elevation evoked by\n \n \n Na\n +<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n removal and the hyperpolarization to histamine. In rat aorta,\n NAGly<\/jats:styled-content>\n opposed the endothelial hyperpolarization and relaxation response to ACh. In unstimulated\n EA<\/jats:styled-content>\n .hy926 cells,\n NAGly<\/jats:styled-content>\n potentiated the whole\u2010cell current attributable to large\u2010conductance\n \n \n Ca\n 2+<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n \u2010activated\n K<\/jats:styled-content>\n +<\/jats:sup>\n (\n \n BK\n Ca<\/jats:sub>\n <\/jats:styled-content>\n ) channels in a\n GDP<\/jats:styled-content>\n \u03b2\n S<\/jats:styled-content>\n \u2010insensitive, paxilline\u2010sensitive manner and produced a sustained hyperpolarization. In cell\u2010free inside\u2010out patches,\n NAGly<\/jats:styled-content>\n stimulated single\n \n BK\n Ca<\/jats:sub>\n <\/jats:styled-content>\n channel activity.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion and Implications<\/jats:title>\n \n Our data showed that\n NCX<\/jats:styled-content>\n is a\n \n \n Ca\n 2+<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n entry pathway in endothelial cells and that\n NAGly<\/jats:styled-content>\n is a potent\n G<\/jats:styled-content>\n \u2010protein\u2010independent modulator of endothelial electrical signalling and has a dual effect on endothelial electrical responses. In agonist pre\u2010stimulated cells,\n NAGly<\/jats:styled-content>\n opposes hyperpolarization and relaxation via inhibition of\n NCX<\/jats:styled-content>\n \u2010mediated\n \n \n Ca\n 2+<\/jats:sup>\n <\/jats:roman>\n <\/jats:styled-content>\n entry, while in unstimulated cells, it promotes hyperpolarization via receptor\u2010independent activation of\n \n BK\n Ca<\/jats:sub>\n <\/jats:styled-content>\n channels.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/bph.12180","type":"journal-article","created":{"date-parts":[[2013,3,20]],"date-time":"2013-03-20T09:49:45Z","timestamp":1363772985000},"page":"933-948","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["N<\/scp>\n \u2010arachidonoyl glycine suppresses\n \n \n Na\n +<\/sup>\n <\/scp>\n <\/scp>\n \/\n \n \n Ca\n 2+<\/sup>\n <\/scp>\n <\/scp>\n exchanger\u2010mediated\n \n \n Ca\n 2+<\/sup>\n <\/scp>\n <\/scp>\n entry into endothelial cells and activates\n \n BK\n Ca<\/sub>\n <\/scp>\n channels independently of\n GPCR<\/scp>\n s"],"prefix":"10.1111","volume":"169","author":[{"given":"Alexander I","family":"Bondarenko","sequence":"first","affiliation":[{"name":"Institute of Molecular Biology and Biochemistry Center of Molecular Medicine Medical University of Graz Graz Austria"},{"name":"Circulatory Physiology Department, A. 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Bogomoletz Institute of Physiology National Academy of Sciences (NAS) of Ukraine Kiev Ukraine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andras T","family":"Deak","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology and Biochemistry Center of Molecular Medicine Medical University of Graz Graz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland","family":"Malli","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology and Biochemistry Center of Molecular Medicine Medical University of Graz Graz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang F","family":"Graier","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology and Biochemistry Center of Molecular Medicine Medical University of Graz Graz 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