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PGF2 increases endothelial nitric oxide synthase in the periphery of the bovine corpus luteum: the possible regulation of blood flow at an early stage of luteolysis

K Shirasuna, Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, 080-8555, Japan
S Watanabe, Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan
T Asahi, Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan
M Wijayagunawardane, Department of Animal Science, University of Peradeniya, University of Peradeniya, Peradeniya , Sri Lanka
K Sasahara, Obihiro, Japan
C Jiang, Omaha, United States
M Matsui, Department of Clinical Veterinary Science, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan
M Sasaki, Department of Basic Veterinary Sciences, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan
T Shimizu, Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan
J Davis, OB/GYN, Univ Nebraska Med Center, Omaha, United States
A Miyamoto, Obihiro, Japan

Correspondence: Koumei Shirasuna, Email: s11079{at}st.obihiro.ac.jp

Abstract

Prostaglandin F2 (PGF2) released from the uterus causes alterations in luteal blood flow, reduces progesterone secretion, and induces luteolysis in the bovine corpus luteum (CL). We have recently discovered that luteal blood flow in periphery of mature CL acutely increases coincidently with pulsatile increases in PGFM (a metabolite of PGF2). In this study, we characterised regional luteal blood flow changes together with regional alterations in endothelial nitric oxide synthase (eNOS) expression during spontaneous luteolysis and in response to PGF2. Smooth muscle actin positive blood vessels larger than 20µm were observed mainly in periphery of mature CL. PGF2 receptor (FPr) was localized to luteal cells and to large blood vessels in periphery of mid CL. PGF2 acutely stimulated eNOS expression in periphery but not in center of mature CL. Injection of the NO donor SNAP into CL induced an acute increase in luteal blood flow and shortened the oestrous cycle. In contrast, injection of the NOS inhibitor L-NAME into CL completely suppressed the acute increase in luteal blood flow induced by PGF2 and delayed the onset of luteolysis. In conclusion, PGF2 has a site-restricted action depending not only on luteal phase but also the region in CL. PGF2 stimulates eNOS expression, vasodilation of blood vessels, and increased luteal blood flow in periphery of mature CL. Furthermore, the increased blood flow is mediated by NO, suggesting that the acute increase in peripheral blood flow to CL is one of the first physiological indicators of NO action in response to PGF2.