title: Prostaglandin F2alpha 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.
abstract: Prostaglandin F(2)(alpha) (PGF(2)(alpha)) 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 the periphery of the mature CL acutely increases coincidently with pulsatile increases in a metabolite of PGF(2)(alpha) (PGFM). In this study, we characterized changes in regional luteal blood flow together with regional alterations in endothelial nitric oxide synthase (eNOS) expression during spontaneous luteolysis and in response to PGF(2)(alpha). Smooth muscle actin-positive blood vessels larger than 20 microm were observed mainly in the periphery of mature CL. PGF(2)(alpha) receptor was localized to luteal cells and large blood vessels in the periphery of mid-CL. PGF(2)(alpha) acutely stimulated eNOS expression in the periphery but not in the center of mature CL. Injection of the NO donor S-nitroso-N-acetylpenicillamine into CL induced an acute increase in luteal blood flow and shortened the estrous cycle. In contrast, injection of the NOS inhibitor l-NAME into CL completely suppressed the acute increase in luteal blood flow induced by PGF(2)(alpha) and delayed the onset of luteolysis. In conclusion, PGF(2)(alpha) has a site-restricted action depending on not only luteal phase but also the region in the CL. PGF(2)(alpha) 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 PGF(2)(alpha).
authors.affiliation: Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro 080-8555, Japan.
authors.forename: Koumei
authors.initials: K
authors.lastname: Shirasuna
authors.forename: Sho
authors.initials: S
authors.lastname: Watanabe
authors.forename: Takayuki
authors.initials: T
authors.lastname: Asahi
authors.forename: Missaka P B
authors.initials: MP
authors.lastname: Wijayagunawardane
authors.forename: Kiemi
authors.initials: K
authors.lastname: Sasahara
authors.forename: Chao
authors.initials: C
authors.lastname: Jiang
authors.forename: Motozumi
authors.initials: M
authors.lastname: Matsui
authors.forename: Motoki
authors.initials: M
authors.lastname: Sasaki
authors.forename: Takashi
authors.initials: T
authors.lastname: Shimizu
authors.forename: John S
authors.initials: JS
authors.lastname: Davis
authors.forename: Akio
authors.initials: A
authors.lastname: Miyamoto
mesh_terms: D000818:Animals; D002417:Cattle; D003338:Corpus Luteum / Q000098:blood supply* / Q000201:enzymology*; D015237:Dinoprost / Q000494:pharmacology*; D005260:Female; D007150:Immunohistochemistry; D007267:Injections; D008183:Luteal Phase / Q000502:physiology*; D003341:Luteolysis; D009131:Muscle, Smooth, Vascular / Q000098:blood supply; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D010396:Penicillamine / Q000031:analogs & derivatives / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D012039:Regional Blood Flow / Q000187:drug effects; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D020030:Nitric Oxide Donors; D012333:RNA, Messenger; C110881:S-nitro-N-acetylpenicillamine; D015237:Dinoprost; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D010396:Penicillamine; D019331:NG-Nitroarginine Methyl Ester