Effect of intraluteal injection of endothelin type A receptor antagonist on PGF2alpha-induced luteolysis in the cow.
Endothelin-1 (ET-1) is a luteolytic mediator in the bovine corpus luteum (CL), and its action appears to be via endothelin type A receptor (ETR-A). Thus, the aim of the present study was to determine the effect of ETR-A antagonist on PGF2alpha-induced luteolysis in the cow. Cows on days 10-12 of the estrous cycle were subjected to five intraluteal injections of the ETR-A antagonist LU 135252 in saline or only saline at -0.5, 2, 4, 6, and 8 h after PGF2alpha administration (=0 h). Serial luteal biopsies were conducted to determine the expression of mRNA in the luteal tissue. There were no significant differences in the decrease in plasma progesterone (P) concentrations and the mRNA expressions of steroidogenic acute regulatory protein and 3beta-hydroxysteroid dehydrogenase/Delta5, Delta4-isomerase between the ETR-A antagonist-treated group and the control group. However, the start of the decline in CL volume and blood flow area surrounding the CL was delayed for almost two days in the ETR-A antagonist-treated group compared to the control group. The mRNA expression of preproET-1 and endothelin type B receptor increased in both groups, while the ETR-A mRNA remained unchanged. In addition, caspase-3 mRNA expression increased significantly at 24 h in the control group only and its level was higher than that of the ETR-A antagonist-treated group. Thus, the present study suggests that ET-1 regulates structural luteolysis via ETR-A by controlling blood vessel contraction in the CL of the cow.
Watanabe
Sho
S
Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Japan.
Shirasuna
Koumei
K
Matsui
Motozumi
M
Yamamoto
Dai
D
Berisha
Bajram
B
Schams
Dieter
D
Miyamoto
Akio
A
D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D002417:Cattle / Q000502:physiology*; D003338:Corpus Luteum / Q000187:drug effects / Q000378:metabolism; D015237:Dinoprost / Q000096:biosynthesis*; D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1 / Q000378:metabolism; D030762:Estrous Cycle / Q000187:drug effects; D005260:Female; D003341:Luteolysis; D008957:Models, Genetic; D012333:RNA, Messenger / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors
D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1; D012333:RNA, Messenger; D012965:Sodium Chloride; D015237:Dinoprost; D015096:3-Hydroxysteroid Dehydrogenases