{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:43:03Z","timestamp":1773420183469,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,9,30]],"date-time":"2004-09-30T00:00:00Z","timestamp":1096502400000},"content-version":"vor","delay-in-days":2556,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1997,10]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>The resting and agonist\u2010stimulated properties of endothelial cells and electrical communication between the endothelium and smooth muscle were investigated in open segments of guinea\u2010pig mesenteric lymphatic vessels using intracellular microelectrodes.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Endothelial cells had a mean resting membrane potential (RMP) of \u2013 71.5 \u00b1 0.5mV (<jats:styled-content><jats:italic>n<\/jats:italic>= 100<\/jats:styled-content>) which was significantly different from the value of \u221260.8 \u00b1 1.1 mV (<jats:styled-content><jats:italic>n<\/jats:italic>= 75<\/jats:styled-content>) recorded in smooth muscle.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Acetylcholine (ACh, 5\u20131 \u03bc<jats:sc>m<\/jats:sc>) generally evoked an initial hyperpolarization followed by depolarization (mean 3.4 \u00b1 0.5 mV and 15.4 \u00b1 1.0 mV, respectively, <jats:styled-content><jats:italic>n<\/jats:italic>= 75<\/jats:styled-content>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Ca<jats:sup>2+<\/jats:sup>\u2010activated K<jats:sup>+<\/jats:sup> channels were likely to underlie the ACh\u2010induced hyperpolarization as this response exhibited an increase in membrane conductance, was larger in 0.5 m<jats:sc>m<\/jats:sc> K<jats:sup>+<\/jats:sup> solution and was blocked by charybdotoxin (50 n<jats:sc>m<\/jats:sc>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The endothelium did not exhibit a response to nitric oxide (NO) as the NO\u2010donor sodium nitroprusside did not alter the RMP and the electrical responses to ACh were not affected by the NO\u2010synthase inhibitor N<jats:sup>\u03c9<\/jats:sup>\u2010nitro L\u2010arginine at a concentration which markedly inhibited smooth muscle hyperpolarization.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Electrical coupling between the endothelium and smooth muscle was not functional as there was extremely limited electrical continuity (1 in 12, endothelial\/smooth muscle cell simultaneous recordings) and bradykinin, noradrenaline and isoprenaline caused different electrical responses in the two cell types.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These results provide the first description of RMP and electrical responses to various agonists in the lymphatic endothelium and its lack of functional electrical coupling with the smooth muscle.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p>","DOI":"10.1111\/j.1469-7793.1997.439be.x","type":"journal-article","created":{"date-parts":[[2004,9,30]],"date-time":"2004-09-30T07:39:25Z","timestamp":1096529965000},"page":"439-451","source":"Crossref","is-referenced-by-count":30,"title":["Functional electrical properties of the endothelium in lymphatic vessels of the guinea\u2010pig mesentery"],"prefix":"10.1113","volume":"504","author":[{"given":"Pierre\u2010Yves","family":"von der Weid","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dirk F.","family":"Van 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