The mechanism and control of rabbit oviduct fluid formation.

The formation of rabbit oviduct fluid was monitored continuously by using an in situ vascular perfusion technique. Oviduct fluid was secreted linearly for at least 3 h at a mean rate of 20.8 ± 1.5 4W/h in estrous does. The rate more than doubled on Day I following mating, was similar to the value at estrus on Day 2, and dropped to 8.3 ,W on Day 3. Dibutyryl cyclic adensine 3’, 5’-monophosphate (cAMP, 1 mM) added to the vascular medium abolished fluid secretion. The same response was obtained, after a lag period, following the addition of cholera toxin (1 mM), forskolin (1 mM), theophylline (1 mM), phorbol dibutyrate (40 pM), A23187 (2 pg/mi), 4-acetamido-4’-isothiocyonatostilbene-2, 2’-disulphonic acid (SITS, 1 mM), and bumetanide (10 pM) to the vascular medium. N-ethylmaleimide (1 mM), which inhibits adenylate cyciase, stimulated oviduct fluid formation. The transmural potential difference (p.d.) across the oviduct was 5.46 ± 1.01 mV. This was increased after cAMP addition to 8.7 ± 1.22 mV. The pd. in oviducts taken 3 days post-ovulation was 7.6 ± 1.75 mV, and was increased by cAMP to 12.7 ± 0.53 mV. Exposure to cholera toxin and forskoiin almost doubled the cAMP content of the oviduct. The undirectional flux of chloride ions from the vascular compartment into the lumen was reduced by about 75% after the addition of cAMP, SITS, and bumetanide. A tentative model to account for the formation and regulation of rabbit oviduct fluid in terms of ion fluxes and cAMP and calcium ion concentrations is presented.