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Experimental Biology and Medicine 228:1057-1062 (2003)
© 2003 Society for Experimental Biology and Medicine


ORIGINAL RESEARCH ARTICLE

Nitric Oxide as a Local Mediator of Prostaglandin F2{alpha}-Induced Regression in Bovine Corpus Luteum: An In Vivo Study

Jerzy J. Jaroszewski*,1, Dariusz J. Skarzynski{dagger} and William Hansel{ddagger}

* Department of Pharmacology, Faculty of Veterinary Medicine, University of Warmia and Mazury in Olsztyn, 10-718 Olsztyn, Poland;
{dagger} Division of Reproductive Endocrinology and Pathophysiology, Institute of Animal Reproduction and Food Research, PAS, Olsztyn, Poland; and
{ddagger} Department of Reproductive Biotechnology, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808

To test whether nitric oxide (NO) is involved in prostaglandin (PG) F2{alpha}-induced regression of the bovine corpus luteum (CL) in vivo, heifers were treated as follows: Group 1, saline (3 ml/h); Group 2, dinoprost, an analogue of prostaglandin F2{alpha} (aPGF2{alpha}; 5 mg/0.5 h); Group III, N{omega}-nitro-L-arginine methyl ester (L-NAME; 200 mg/4 h), an inhibitor of nitric oxide synthase; and Group IV, L-NAME (400 mg/4 h) and aPGF2{alpha} (5 mg/0.5 h). All treatments were administered by an intraluteal microdialysis system (MDS) on day 15 of the cycle. Perfusate and jugular plasma samples were collected at half-hour intervals; additionally, jugular plasma samples were collected once daily from day 16 to day 21 of the cycle. In the perfusate samples, aPGF2{alpha} increased P4 (P < 0.05), PGE2 (P < 0.001), and LTC4 (P < 0.05) concentrations; L-NAME increased P4 (P < 0.05) but did not change PGE2 and LTC4 (P > 0.05) concentrations as compared with the period before treatment. Simultaneous perfusion of CL with L-NAME and aPGF2{alpha} caused a further increase of P4 concentration (P < 0.05) induced by L-NAME or aPGF2{alpha} treatment and increased PGE2 and LTC4 (P < 0.001) concentrations to the level observed after aPGF2{alpha} treatment. Perfusion of CL with aPGF2{alpha} caused luteal regression within 24 h, while perfusion with L-NAME prolonged the life span of CL to day 21 (P < 0.05). Concomitant L-NAME and aPGF2{alpha} treatment partially counteracted (P < 0.05) the luteal regression caused by aPGF2{alpha} administration. These results show that NO is involved in the process of luteolysis in the bovine CL and suggest that the luteolytic effect of aPGF2{alpha} may be mediated by NO as an important component of an autocrine/paracrine luteolytic cascade.

Key Words: nitric oxide • progesterone • prostaglandins • corpus luteum • bovine




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