Abstract

The effects of noradrenaline (NA) and nitric oxide (NO) on prostaglandins (PGs) and progesterone (P4) secretion during the development of the bovine corpus luteum (CL) were investigated. Bovine luteal cells of early and mid-cycle CL were cultured for 20 to 24 h in medium containing 10% calf serum, washed, and treated with NA or nitrergic agents for an additional 16 h in a serum-free medium. NA (10 −5 M) stimulated P4 from early and mid-cycle CL by 238% and 154% ( P < 0.01), respectively. Moreover, although NA induced a twofold increase in PGE 2 secretion ( P < 0.01) in both examined periods, the effect of NA on PGF 2α secretion was approximately 1.5 times higher ( P < 0.05) in early than in mid-cycle CL. Two NO synthase inhibitors, l-NAME and l-NOARG (both 10 −4 M), stimulated P4 secretion only in mid-luteal cells ( P < 0.01), although they did not affect the cells from early CL. Although a NO donor, S-NAP (10 −4 M) inhibited P4 secretion from mid-cycle luteal cells ( P < 0.05), it strongly stimulated PGE 2 in both examined phases ( P < 0.001). On the other hand, the output of PGF 2α was stimulated by S-NAP only in the cells of the mid-cycle CL ( P < 0.01). The overall results suggest that adrenergic and nitrergic agents play opposite roles in the regulation of bovine CL functions. Whereas NA may play a supporting role in luteal development, NO may participate in the functional regression of the bovine CL by inhibiting steroidogenesis.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.