Endothelin-1 within the corpus luteum during spontaneous luteolysis in the cow: local interaction with prostaglandin F2alpha and angiotensin II.
It is generally accepted that endothelin-1 (ET-1) is involved in the regression of the corpus luteum (CL) in cows, but there are few in vivo data available on the local release of vasoconstrictors, including ET-1. Thus, we aimed to determine in detail the local secretion of ET-1, angiotensin II (Ang II) and prostaglandin F2alpha (PGF2alpha) within the CL during spontaneous luteolysis in the cow. To observe real-time dynamics of the releasing profile of CL-derived factors, a microdialysis system was surgically implanted in the CL on day 15 of the estrous cycle and continuously perfused with Ringer's solution. Local secretion of ET-1, Ang II and PGF2alpha increased immediately after the onset of luteolysis (the time point when progesterone release started to decrease within the CL) and was maintained at high levels. A positive relationship was observed in intra-luteal changes among ET-1, Ang II and PGF2alpha release. This is the first real-time and in vivo evidence that the secretion of ET-1 together with Ang II and PGF2alpha immediately increases within the CL after the onset of spontaneous luteolysis. Consequently, we suggest that the activation of a local positive feedback mechanism among ET-1, Ang II and PGF2alpha might play a functional role in the paracrine modulation of luteolytic cascade and, simultaneously, the elevated ET-1 with Ang II and PGF2alpha should induce a strong vasoconstriction, thereby reducing the blood supplying the CL during spontaneous luteolysis.
Shirasuna
Koumei
K
Department of Agricultural and Life Science, Obihiro University of Agriculture andVeterinary Medicine, Japan.
Asaoka
Hitomi
H
Acosta
Tomas J
TJ
Wijayagunawardane
Missaka P B
MP
Matsui
Motozumi
M
Ohtani
Masayuki
M
Miyamoto
Akio
A
D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D002417:Cattle; D003338:Corpus Luteum / Q000378:metabolism*; D015237:Dinoprost / Q000378:metabolism*; D019332:Endothelin-1 / Q000378:metabolism*; D025461:Feedback, Physiological; D005260:Female; D003341:Luteolysis; D017551:Microdialysis; D019899:Paracrine Communication; D011374:Progesterone / Q000378:metabolism; D013997:Time Factors
D019332:Endothelin-1; D000804:Angiotensin II; D011374:Progesterone; D015237:Dinoprost