{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T19:55:10Z","timestamp":1792439710343,"version":"4.5.0"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2002,2,1]],"date-time":"2002-02-01T00:00:00Z","timestamp":1012521600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2002,2]]},"abstract":"<jats:p>Short chain fatty acids, including propionate, are generated in the caecum and large intestine, and when absorbed may elicit localised increases in intestinal blood flow. We sought to assess the mechanism by which propionate caused vasorelaxation. Propionate\u2010mediated relaxation of noradrenaline\u2010preconstricted rat mesenteric small arteries (RMSAs, i.d. 200\u2013300 \u03bcm) was studied using small vessel myography. Propionate (1\u201330 m<jats:sc>m<\/jats:sc>) produced a concentration\u2010dependent relaxation. Relaxation induced by 10 m<jats:sc>m<\/jats:sc> propionate (the approximate EC<jats:sub>50<\/jats:sub>) was almost abolished by endothelial denudation, although a marked relaxation to a very high concentration of propionate (50 m<jats:sc>m<\/jats:sc>) persisted in the absence of the endothelium. In endothelium\u2010intact RMSAs, relaxation to 10 m<jats:sc>m<\/jats:sc> propionate was almost abolished by elevating [K<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub> to 25 m<jats:sc>m<\/jats:sc>, but was unaffected by 100 \u03bc<jats:sc>m<\/jats:sc><jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>\u2010nitro\u2010<jats:sc>l<\/jats:sc>\u2010arginine methyl ester (<jats:sc>l<\/jats:sc>\u2010NAME) (68 \u00b1 4 <jats:italic>vs<\/jats:italic>. 66 \u00b1 3 % in controls, <jats:italic>n<\/jats:italic>= 35), or by 1 \u03bc<jats:sc>m<\/jats:sc> indomethacin (60 \u00b1 4 <jats:italic>vs<\/jats:italic>. 61 \u00b1 7 % in controls, <jats:italic>n<\/jats:italic>= 15). In the presence of <jats:sc>l<\/jats:sc>\u2010NAME, relaxation to 10 m<jats:sc>m<\/jats:sc> propionate was significantly and markedly (i.e. &gt; 50 %) inhibited by 50 \u03bc<jats:sc>m<\/jats:sc> Ba<jats:sup>2+<\/jats:sup> and by the combination of 100 n<jats:sc>m<\/jats:sc> charybdotoxin and 100 n<jats:sc>m<\/jats:sc> apamin. A similar effect on propionate\u2010mediated relaxation was also exerted by 100 \u03bc<jats:sc>m<\/jats:sc> ouabain, and by the combination of 50 \u03bc<jats:sc>m<\/jats:sc> barium with ouabain. Relaxation was also significantly and markedly inhibited by pre\u2010treatment of RMSAs with 100 n<jats:sc>m<\/jats:sc> thapsigargin or 10 \u03bc<jats:sc>m<\/jats:sc> cyclopiazonic acid (CPA). The results demonstrate that 10 m<jats:sc>m<\/jats:sc> propionate relaxes RMSAs via endothelium\u2010derived hyperpolarising factor (EDHF). The observation that relaxation by propionate is inhibited by thapsigargin and CPA suggests that this action of propionate involves the release of endothelial cell Ca<jats:sup>2+<\/jats:sup> stores.<\/jats:p>","DOI":"10.1113\/jphysiol.2001.013105","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:45:57Z","timestamp":1027773957000},"page":"879-890","source":"Crossref","is-referenced-by-count":27,"title":["Propionate\u2010induced relaxation in rat mesenteric arteries: a role for endothelium\u2010derived hyperpolarising factor"],"prefix":"10.1113","volume":"538","author":[{"given":"G.","family":"Knock","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Psaroudakis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Abbot","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. 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