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Blood flow: A key regulatory component of corpus luteum function in the cow
Prostaglandin F2α (PGF 2α) is the primary luteolysin in the cow. During the early luteal phase, the corpus luteum (CL) is resistant to the luteolytic effect of PGF 2α. Once mature, the CL becomes responsive to PGF 2α and undergoes luteal regression. These actions of PGF 2α coincide with changes in l...
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Published in: | Domestic animal endocrinology 2005-08, Vol.29 (2), p.329-339 |
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description | Prostaglandin F2α (PGF
2α) is the primary luteolysin in the cow. During the early luteal phase, the corpus luteum (CL) is resistant to the luteolytic effect of PGF
2α. Once mature, the CL becomes responsive to PGF
2α and undergoes luteal regression. These actions of PGF
2α coincide with changes in luteal blood flow (BF): PGF
2α has no effect on BF in the early CL, but acutely increases BF in the peripheral vasculature of the mature CL within 30
min of PGF
2α injection. During spontaneous luteolysis, luteal BF increases on Days 17–18 of the estrous cycle, prior to any decrease in plasma progesterone (P). The increase in luteal BF is synchronous with an increase in plasma PGFM levels, suggesting that pulsatile release of PGF
2α from uterus stimulates the increase in luteal BF. Serial biopsies of these CL showed that mRNA expression for endothelial nitric oxide synthase (eNOS) together with endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) increases on Days 17–18 when the luteal BF is elevated. On Day 19 when plasma P level firstly decreases, eNOS mRNA returns to the basal level whereas ET-1 and ACE mRNA remains elevated. Cyclooxygenase-2 (COX-2) mRNA expression increases on Day 19. In support of these data, an in vivo microdialysis study revealed that luteal ET-1 and angiotensin II (Ang II) secretion increases and precedes PGF
2α secretion during spontaneous luteolysis. In conclusion, we show for the first time that an acute increase of BF occurs in the peripheral vasculature of the mature CL together with increases in eNOS expression and ET-1 and Ang II secretion in the CL during the early stages of luteolysis in the cow. We propose that the increase in luteal BF may be induced by NO from large arterioles surrounding the CL, and simultaneously uterine or exogenous PGF
2α directly increases ET-1 and Ang II secretion from endothelial cells of microcapillary vessels within the CL, thereby suppressing P secretion by luteal cells. Taken together, our results indicate that an acute increase in luteal BF occurs as a first step of luteolysis in response to PGF
2α. Therefore, local BF plays a key role to initiate luteal regression in the cow. |
doi_str_mv | 10.1016/j.domaniend.2005.03.011 |
format | article |
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2α) is the primary luteolysin in the cow. During the early luteal phase, the corpus luteum (CL) is resistant to the luteolytic effect of PGF
2α. Once mature, the CL becomes responsive to PGF
2α and undergoes luteal regression. These actions of PGF
2α coincide with changes in luteal blood flow (BF): PGF
2α has no effect on BF in the early CL, but acutely increases BF in the peripheral vasculature of the mature CL within 30
min of PGF
2α injection. During spontaneous luteolysis, luteal BF increases on Days 17–18 of the estrous cycle, prior to any decrease in plasma progesterone (P). The increase in luteal BF is synchronous with an increase in plasma PGFM levels, suggesting that pulsatile release of PGF
2α from uterus stimulates the increase in luteal BF. Serial biopsies of these CL showed that mRNA expression for endothelial nitric oxide synthase (eNOS) together with endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) increases on Days 17–18 when the luteal BF is elevated. On Day 19 when plasma P level firstly decreases, eNOS mRNA returns to the basal level whereas ET-1 and ACE mRNA remains elevated. Cyclooxygenase-2 (COX-2) mRNA expression increases on Day 19. In support of these data, an in vivo microdialysis study revealed that luteal ET-1 and angiotensin II (Ang II) secretion increases and precedes PGF
2α secretion during spontaneous luteolysis. In conclusion, we show for the first time that an acute increase of BF occurs in the peripheral vasculature of the mature CL together with increases in eNOS expression and ET-1 and Ang II secretion in the CL during the early stages of luteolysis in the cow. We propose that the increase in luteal BF may be induced by NO from large arterioles surrounding the CL, and simultaneously uterine or exogenous PGF
2α directly increases ET-1 and Ang II secretion from endothelial cells of microcapillary vessels within the CL, thereby suppressing P secretion by luteal cells. Taken together, our results indicate that an acute increase in luteal BF occurs as a first step of luteolysis in response to PGF
2α. Therefore, local BF plays a key role to initiate luteal regression in the cow.</description><identifier>ISSN: 0739-7240</identifier><identifier>EISSN: 1879-0054</identifier><identifier>DOI: 10.1016/j.domaniend.2005.03.011</identifier><identifier>PMID: 15888379</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiotensin II - secretion ; Animals ; Blood Flow Velocity ; Cattle - physiology ; Corpus Luteum - blood supply ; Corpus Luteum - physiology ; Dinoprost - analogs & derivatives ; Dinoprost - blood ; Dinoprost - physiology ; Endothelin-1 - genetics ; Female ; Gene Expression ; Local blood flow ; Luteolysis ; Luteolysis - physiology ; Nitric oxide ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase Type III ; Peptidyl-Dipeptidase A - genetics ; Prostaglandin F2α ; RNA, Messenger - analysis ; Vasoactive peptides</subject><ispartof>Domestic animal endocrinology, 2005-08, Vol.29 (2), p.329-339</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-4f5d7b0a3f9003ef6d130f4ad2ede756c7d948dfbda0ac1cf58ff24e6a3c89343</citedby><cites>FETCH-LOGICAL-c435t-4f5d7b0a3f9003ef6d130f4ad2ede756c7d948dfbda0ac1cf58ff24e6a3c89343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15888379$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miyamoto, A.</creatorcontrib><creatorcontrib>Shirasuna, K.</creatorcontrib><creatorcontrib>Wijayagunawardane, M.P.B.</creatorcontrib><creatorcontrib>Watanabe, S.</creatorcontrib><creatorcontrib>Hayashi, M.</creatorcontrib><creatorcontrib>Yamamoto, D.</creatorcontrib><creatorcontrib>Matsui, M.</creatorcontrib><creatorcontrib>Acosta, T.J.</creatorcontrib><title>Blood flow: A key regulatory component of corpus luteum function in the cow</title><title>Domestic animal endocrinology</title><addtitle>Domest Anim Endocrinol</addtitle><description>Prostaglandin F2α (PGF
2α) is the primary luteolysin in the cow. During the early luteal phase, the corpus luteum (CL) is resistant to the luteolytic effect of PGF
2α. Once mature, the CL becomes responsive to PGF
2α and undergoes luteal regression. These actions of PGF
2α coincide with changes in luteal blood flow (BF): PGF
2α has no effect on BF in the early CL, but acutely increases BF in the peripheral vasculature of the mature CL within 30
min of PGF
2α injection. During spontaneous luteolysis, luteal BF increases on Days 17–18 of the estrous cycle, prior to any decrease in plasma progesterone (P). The increase in luteal BF is synchronous with an increase in plasma PGFM levels, suggesting that pulsatile release of PGF
2α from uterus stimulates the increase in luteal BF. Serial biopsies of these CL showed that mRNA expression for endothelial nitric oxide synthase (eNOS) together with endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) increases on Days 17–18 when the luteal BF is elevated. On Day 19 when plasma P level firstly decreases, eNOS mRNA returns to the basal level whereas ET-1 and ACE mRNA remains elevated. Cyclooxygenase-2 (COX-2) mRNA expression increases on Day 19. In support of these data, an in vivo microdialysis study revealed that luteal ET-1 and angiotensin II (Ang II) secretion increases and precedes PGF
2α secretion during spontaneous luteolysis. In conclusion, we show for the first time that an acute increase of BF occurs in the peripheral vasculature of the mature CL together with increases in eNOS expression and ET-1 and Ang II secretion in the CL during the early stages of luteolysis in the cow. We propose that the increase in luteal BF may be induced by NO from large arterioles surrounding the CL, and simultaneously uterine or exogenous PGF
2α directly increases ET-1 and Ang II secretion from endothelial cells of microcapillary vessels within the CL, thereby suppressing P secretion by luteal cells. Taken together, our results indicate that an acute increase in luteal BF occurs as a first step of luteolysis in response to PGF
2α. Therefore, local BF plays a key role to initiate luteal regression in the cow.</description><subject>Angiotensin II - secretion</subject><subject>Animals</subject><subject>Blood Flow Velocity</subject><subject>Cattle - physiology</subject><subject>Corpus Luteum - blood supply</subject><subject>Corpus Luteum - physiology</subject><subject>Dinoprost - analogs & derivatives</subject><subject>Dinoprost - blood</subject><subject>Dinoprost - physiology</subject><subject>Endothelin-1 - genetics</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Local blood flow</subject><subject>Luteolysis</subject><subject>Luteolysis - physiology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Prostaglandin F2α</subject><subject>RNA, Messenger - analysis</subject><subject>Vasoactive peptides</subject><issn>0739-7240</issn><issn>1879-0054</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkMtOwzAQRS0EgvL4BfCKXcK4TmKHXUG8BBIbWFuuPYaUJC52QtW_x6gVLFmNZubeO5pDyBmDnAGrLha59Z3uG-xtPgUoc-A5MLZDJkyKOkuTYpdMQPA6E9MCDshhjAsAEMm9Tw5YKaXkop6Qx6vWe0td61eXdEY_cE0Dvo2tHnxYU-O7pe-xH6h3qQnLMdJ2HHDsqBt7MzS-p01Ph3dM29Ux2XO6jXiyrUfk9fbm5fo-e3q-e7iePWWm4OWQFa60Yg6auxqAo6ss4-AKbadoUZSVEbYupHVzq0EbZlwpnZsWWGluZM0LfkTON7nL4D9HjIPqmmiwbXWPfoyqkgAVSJ6EYiM0wccY0KllaDod1oqB-uGoFuqXo_rhqICrxDE5T7cnxnmH9s-3BZcEs40A06NfDQYVTUoxaJuAZkixzb9HvgFUVolj</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>Miyamoto, A.</creator><creator>Shirasuna, K.</creator><creator>Wijayagunawardane, M.P.B.</creator><creator>Watanabe, S.</creator><creator>Hayashi, M.</creator><creator>Yamamoto, D.</creator><creator>Matsui, M.</creator><creator>Acosta, T.J.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20050801</creationdate><title>Blood flow: A key regulatory component of corpus luteum function in the cow</title><author>Miyamoto, A. ; Shirasuna, K. ; Wijayagunawardane, M.P.B. ; Watanabe, S. ; Hayashi, M. ; Yamamoto, D. ; Matsui, M. ; Acosta, T.J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-4f5d7b0a3f9003ef6d130f4ad2ede756c7d948dfbda0ac1cf58ff24e6a3c89343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Angiotensin II - secretion</topic><topic>Animals</topic><topic>Blood Flow Velocity</topic><topic>Cattle - physiology</topic><topic>Corpus Luteum - blood supply</topic><topic>Corpus Luteum - physiology</topic><topic>Dinoprost - analogs & derivatives</topic><topic>Dinoprost - blood</topic><topic>Dinoprost - physiology</topic><topic>Endothelin-1 - genetics</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Local blood flow</topic><topic>Luteolysis</topic><topic>Luteolysis - physiology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Prostaglandin F2α</topic><topic>RNA, Messenger - analysis</topic><topic>Vasoactive peptides</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miyamoto, A.</creatorcontrib><creatorcontrib>Shirasuna, K.</creatorcontrib><creatorcontrib>Wijayagunawardane, M.P.B.</creatorcontrib><creatorcontrib>Watanabe, S.</creatorcontrib><creatorcontrib>Hayashi, M.</creatorcontrib><creatorcontrib>Yamamoto, D.</creatorcontrib><creatorcontrib>Matsui, M.</creatorcontrib><creatorcontrib>Acosta, T.J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Domestic animal endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miyamoto, A.</au><au>Shirasuna, K.</au><au>Wijayagunawardane, M.P.B.</au><au>Watanabe, S.</au><au>Hayashi, M.</au><au>Yamamoto, D.</au><au>Matsui, M.</au><au>Acosta, T.J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blood flow: A key regulatory component of corpus luteum function in the cow</atitle><jtitle>Domestic animal endocrinology</jtitle><addtitle>Domest Anim Endocrinol</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>29</volume><issue>2</issue><spage>329</spage><epage>339</epage><pages>329-339</pages><issn>0739-7240</issn><eissn>1879-0054</eissn><abstract>Prostaglandin F2α (PGF
2α) is the primary luteolysin in the cow. During the early luteal phase, the corpus luteum (CL) is resistant to the luteolytic effect of PGF
2α. Once mature, the CL becomes responsive to PGF
2α and undergoes luteal regression. These actions of PGF
2α coincide with changes in luteal blood flow (BF): PGF
2α has no effect on BF in the early CL, but acutely increases BF in the peripheral vasculature of the mature CL within 30
min of PGF
2α injection. During spontaneous luteolysis, luteal BF increases on Days 17–18 of the estrous cycle, prior to any decrease in plasma progesterone (P). The increase in luteal BF is synchronous with an increase in plasma PGFM levels, suggesting that pulsatile release of PGF
2α from uterus stimulates the increase in luteal BF. Serial biopsies of these CL showed that mRNA expression for endothelial nitric oxide synthase (eNOS) together with endothelin-1 (ET-1) and angiotensin converting enzyme (ACE) increases on Days 17–18 when the luteal BF is elevated. On Day 19 when plasma P level firstly decreases, eNOS mRNA returns to the basal level whereas ET-1 and ACE mRNA remains elevated. Cyclooxygenase-2 (COX-2) mRNA expression increases on Day 19. In support of these data, an in vivo microdialysis study revealed that luteal ET-1 and angiotensin II (Ang II) secretion increases and precedes PGF
2α secretion during spontaneous luteolysis. In conclusion, we show for the first time that an acute increase of BF occurs in the peripheral vasculature of the mature CL together with increases in eNOS expression and ET-1 and Ang II secretion in the CL during the early stages of luteolysis in the cow. We propose that the increase in luteal BF may be induced by NO from large arterioles surrounding the CL, and simultaneously uterine or exogenous PGF
2α directly increases ET-1 and Ang II secretion from endothelial cells of microcapillary vessels within the CL, thereby suppressing P secretion by luteal cells. Taken together, our results indicate that an acute increase in luteal BF occurs as a first step of luteolysis in response to PGF
2α. Therefore, local BF plays a key role to initiate luteal regression in the cow.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15888379</pmid><doi>10.1016/j.domaniend.2005.03.011</doi><tpages>11</tpages></addata></record> |
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source | ScienceDirect Freedom Collection 2022-2024 |
subjects | Angiotensin II - secretion Animals Blood Flow Velocity Cattle - physiology Corpus Luteum - blood supply Corpus Luteum - physiology Dinoprost - analogs & derivatives Dinoprost - blood Dinoprost - physiology Endothelin-1 - genetics Female Gene Expression Local blood flow Luteolysis Luteolysis - physiology Nitric oxide Nitric Oxide Synthase - genetics Nitric Oxide Synthase Type III Peptidyl-Dipeptidase A - genetics Prostaglandin F2α RNA, Messenger - analysis Vasoactive peptides |
title | Blood flow: A key regulatory component of corpus luteum function in the cow |
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