A new role for bicarbonate secretion in cervico-uterine mucus release

Authors

  • Ruth W. Muchekehu,

    1. Department of Pediatrics-0830, School of Medicine, University of California–San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0831, USA
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  • Paul M. Quinton

    1. Department of Pediatrics-0830, School of Medicine, University of California–San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0831, USA
    2. Division of Biomedical Sciences, University of California–Riverside, Riverside, CA 92507-0121, USA
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Corresponding author P. M. Quinton: Department of Pediatrics-0830, School of Medicine, University of California–San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0830, USA. Email: pquinton@ucsd.edu

Abstract

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 (HCO3) secretion. Prostaglandin E2 (PGE2)- and carbachol-stimulated mucus release was severely inhibited in the absence of serosal HCO3, HCO3 transport, or functional cystic fibrosis transmembrane conductance regulator (CFTR). In contrast to mucus release, PGE2- and carbachol-stimulated 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 ΔF508 reproductive tract, even though stimulated fluid secretion was preserved. Thus, CFTR mutations and/or poor bicarbonate secretion may be associated with reduced female fertility associated with abnormal mucus and specifically, may account for the increased viscosity and lack of cyclical changes in cervical mucus long noted in women with cystic fibrosis.

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