{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T02:40:40Z","timestamp":1791168040960,"version":"4.1.0"},"reference-count":90,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2010,6,29]],"date-time":"2010-06-29T00:00:00Z","timestamp":1277769600000},"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":[[2010,7]]},"abstract":"<jats:p>Cervical mucus thinning and release during the female reproductive cycle is thought to rely mainly on fluid secretion. However, we now find that mucus released from the murine reproductive tract critically depends upon concurrent bicarbonate (HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>) secretion. Prostaglandin E<jats:sub>2<\/jats:sub>(PGE<jats:sub>2<\/jats:sub>)\u2010 and carbachol\u2010stimulated mucus release was severely inhibited in the absence of serosal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>, HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>transport, or functional cystic fibrosis transmembrane conductance regulator (CFTR). In contrast to mucus release, PGE<jats:sub>2<\/jats:sub>\u2010 and carbachol\u2010stimulated fluid secretion was not dependent on bicarbonate or on CFTR, but was completely blocked by niflumic acid. We found stimulated mucus release was severely impaired in the cystic fibrosis \u0394F508 reproductive tract, even though stimulated fluid secretion was preserved. 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