Improvement of vascular function by acute and chronic treatment with the GPR30 agonist G1 in experimental diabetes mellitus
The G-protein coupled estrogen receptor 30 (GPR30) is a seven-transmembrane domain receptor that mediates rapid estrogen responses in a wide variety of cell types. This receptor is highly expressed in the cardiovascular system, and exerts vasodilatory effects. The objective of the present study was...
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| Veröffentlicht in: | PloS one 2012-06, Vol.7 (6), p.e38787-e38787 |
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| description | The G-protein coupled estrogen receptor 30 (GPR30) is a seven-transmembrane domain receptor that mediates rapid estrogen responses in a wide variety of cell types. This receptor is highly expressed in the cardiovascular system, and exerts vasodilatory effects. The objective of the present study was to investigate the effects of GPR30 on vascular responsiveness in diabetic ovariectomized (OVX) rats and elucidate the possible mechanism involved. The roles of GPR30 were evaluated in the thoracic aorta and cultured endothelial cells. The GPR30 agonist G1 induced a dose-dependent vasodilation in the thoracic aorta of the diabetic OVX rats, which was partially attenuated by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methylester (L-NAME) and the GPR30-selective antagonist G15. Dose-dependent vasoconstrictive responses to phenylephrine were attenuated significantly in the rings of the thoracic aorta following the acute G1 administration in the diabetic OVX rats. This effect of G1 was abolished partially by L-NAME and G15. The acute administration of G1 increased significantly the eNOS activity and the concentration of NO in the endothelial cells exposed to high glucose. G1 treatment induced an enhanced endothelium-dependent relaxation to acetylcholine (Ach) in the diabetic OVX rats. Further examination revealed that G1 induced vasodilation in the diabetic OVX rats by increasing the phosphorylation of eNOS. These findings provide preliminary evidence that GPR30 activation leads to eNOS activation, as well as vasodilation, to a certain degree and has beneficial effects on vascular function in diabetic OVX rats. |
| doi_str_mv | 10.1371/journal.pone.0038787 |
| format | Article |
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This receptor is highly expressed in the cardiovascular system, and exerts vasodilatory effects. The objective of the present study was to investigate the effects of GPR30 on vascular responsiveness in diabetic ovariectomized (OVX) rats and elucidate the possible mechanism involved. The roles of GPR30 were evaluated in the thoracic aorta and cultured endothelial cells. The GPR30 agonist G1 induced a dose-dependent vasodilation in the thoracic aorta of the diabetic OVX rats, which was partially attenuated by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methylester (L-NAME) and the GPR30-selective antagonist G15. Dose-dependent vasoconstrictive responses to phenylephrine were attenuated significantly in the rings of the thoracic aorta following the acute G1 administration in the diabetic OVX rats. This effect of G1 was abolished partially by L-NAME and G15. The acute administration of G1 increased significantly the eNOS activity and the concentration of NO in the endothelial cells exposed to high glucose. G1 treatment induced an enhanced endothelium-dependent relaxation to acetylcholine (Ach) in the diabetic OVX rats. Further examination revealed that G1 induced vasodilation in the diabetic OVX rats by increasing the phosphorylation of eNOS. These findings provide preliminary evidence that GPR30 activation leads to eNOS activation, as well as vasodilation, to a certain degree and has beneficial effects on vascular function in diabetic OVX rats.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0038787</identifier><identifier>PMID: 22679517</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetylcholine ; Activation ; Animals ; Aorta ; Arginine ; Biology ; Blood Glucose - drug effects ; Body Weight - drug effects ; Cardiovascular system ; Diabetes mellitus ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes therapy ; Endothelial cells ; Endothelium ; Estrogens ; Female ; Glucose ; Hypoglycemic Agents - therapeutic use ; Insulin - blood ; Kinases ; Medicine ; Menopause ; NG-Nitroarginine methyl ester ; Nitric oxide ; Nitric Oxide - blood ; Nitric-oxide synthase ; Ovariectomy ; Phenylephrine ; Phosphorylation ; Rats ; Receptors, G-Protein-Coupled - agonists ; Rodents ; Thorax ; Type 2 diabetes ; Vasodilation ; Vasodilator agents</subject><ispartof>PloS one, 2012-06, Vol.7 (6), p.e38787-e38787</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Li et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d8525a438dccb030f0f813ab68621607cdea2c14a3128bb94d57102f45c00a833</citedby><cites>FETCH-LOGICAL-c692t-d8525a438dccb030f0f813ab68621607cdea2c14a3128bb94d57102f45c00a833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367949/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367949/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22679517$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cignarella, Andrea</contributor><creatorcontrib>Li, Zi-lin</creatorcontrib><creatorcontrib>Liu, Jin-cheng</creatorcontrib><creatorcontrib>Liu, Shui-bing</creatorcontrib><creatorcontrib>Li, Xiao-qiang</creatorcontrib><creatorcontrib>Yi, Ding-hua</creatorcontrib><creatorcontrib>Zhao, Ming-gao</creatorcontrib><title>Improvement of vascular function by acute and chronic treatment with the GPR30 agonist G1 in experimental diabetes mellitus</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The G-protein coupled estrogen receptor 30 (GPR30) is a seven-transmembrane domain receptor that mediates rapid estrogen responses in a wide variety of cell types. This receptor is highly expressed in the cardiovascular system, and exerts vasodilatory effects. The objective of the present study was to investigate the effects of GPR30 on vascular responsiveness in diabetic ovariectomized (OVX) rats and elucidate the possible mechanism involved. The roles of GPR30 were evaluated in the thoracic aorta and cultured endothelial cells. The GPR30 agonist G1 induced a dose-dependent vasodilation in the thoracic aorta of the diabetic OVX rats, which was partially attenuated by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methylester (L-NAME) and the GPR30-selective antagonist G15. Dose-dependent vasoconstrictive responses to phenylephrine were attenuated significantly in the rings of the thoracic aorta following the acute G1 administration in the diabetic OVX rats. This effect of G1 was abolished partially by L-NAME and G15. The acute administration of G1 increased significantly the eNOS activity and the concentration of NO in the endothelial cells exposed to high glucose. G1 treatment induced an enhanced endothelium-dependent relaxation to acetylcholine (Ach) in the diabetic OVX rats. Further examination revealed that G1 induced vasodilation in the diabetic OVX rats by increasing the phosphorylation of eNOS. These findings provide preliminary evidence that GPR30 activation leads to eNOS activation, as well as vasodilation, to a certain degree and has beneficial effects on vascular function in diabetic OVX rats.</description><subject>Acetylcholine</subject><subject>Activation</subject><subject>Animals</subject><subject>Aorta</subject><subject>Arginine</subject><subject>Biology</subject><subject>Blood Glucose - drug effects</subject><subject>Body Weight - drug effects</subject><subject>Cardiovascular system</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes therapy</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Estrogens</subject><subject>Female</subject><subject>Glucose</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin - blood</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Menopause</subject><subject>NG-Nitroarginine methyl ester</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - blood</subject><subject>Nitric-oxide synthase</subject><subject>Ovariectomy</subject><subject>Phenylephrine</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Rodents</subject><subject>Thorax</subject><subject>Type 2 diabetes</subject><subject>Vasodilation</subject><subject>Vasodilator agents</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7jr6D0QDgujFjPlq2t4Iy6LjwMLK-nEbTtN0mqHTjEk67uKfN93pLlPZCwklJXne9-Sc5CTJS4IXhGXkw8b2roN2sbOdXmDM8izPHiWnpGB0Lihmj4_-T5Jn3m8wTlkuxNPkhFKRFSnJTpM_q-3O2b3e6i4gW6M9eNW34FDddyoY26HyBoHqg0bQVUg1znZGoeA0hFvNbxMaFBqNll-vGEawjvs-oCVBpkP6eqedGThoUWWg1EF7tNVta0LvnydPami9fjHOs-TH50_fz7_MLy6Xq_Ozi7kSBQ3zKk9pCpzllVIlZrjGdU4YlCIXlAicqUoDVYQDIzQvy4JXaUYwrXmqMIacsVny-uC7a62XY928JIymmHKGRSRWB6KysJG7eGRwN9KCkbcL1q0luGBUqyWBStUFA6JIyWuFS8K5iNEqoGn88uj1cYzWl1tdqZi8g3ZiOt3pTCPXdi8Zi5fCi2jwbjRw9levfZBb41WsGXTa9vHcmBSCMMaHzN78gz6c3UitISZgutrGuGowlWc8ywgRPIKzZPEAFUelt0bFR1abuD4RvJ8IIhP0dVhD771cfbv6f_by55R9e8Q2GtrQeNv2w2v0U5AfQOWs907X90UmWA49clcNOfSIHHskyl4dX9C96K4p2F-85gx3</recordid><startdate>20120605</startdate><enddate>20120605</enddate><creator>Li, Zi-lin</creator><creator>Liu, Jin-cheng</creator><creator>Liu, Shui-bing</creator><creator>Li, Xiao-qiang</creator><creator>Yi, Ding-hua</creator><creator>Zhao, Ming-gao</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120605</creationdate><title>Improvement of vascular function by acute and chronic treatment with the GPR30 agonist G1 in experimental diabetes mellitus</title><author>Li, Zi-lin ; Liu, Jin-cheng ; Liu, Shui-bing ; Li, Xiao-qiang ; Yi, Ding-hua ; Zhao, Ming-gao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-d8525a438dccb030f0f813ab68621607cdea2c14a3128bb94d57102f45c00a833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetylcholine</topic><topic>Activation</topic><topic>Animals</topic><topic>Aorta</topic><topic>Arginine</topic><topic>Biology</topic><topic>Blood Glucose - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Zi-lin</au><au>Liu, Jin-cheng</au><au>Liu, Shui-bing</au><au>Li, Xiao-qiang</au><au>Yi, Ding-hua</au><au>Zhao, Ming-gao</au><au>Cignarella, Andrea</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Improvement of vascular function by acute and chronic treatment with the GPR30 agonist G1 in experimental diabetes mellitus</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-06-05</date><risdate>2012</risdate><volume>7</volume><issue>6</issue><spage>e38787</spage><epage>e38787</epage><pages>e38787-e38787</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The G-protein coupled estrogen receptor 30 (GPR30) is a seven-transmembrane domain receptor that mediates rapid estrogen responses in a wide variety of cell types. This receptor is highly expressed in the cardiovascular system, and exerts vasodilatory effects. The objective of the present study was to investigate the effects of GPR30 on vascular responsiveness in diabetic ovariectomized (OVX) rats and elucidate the possible mechanism involved. The roles of GPR30 were evaluated in the thoracic aorta and cultured endothelial cells. The GPR30 agonist G1 induced a dose-dependent vasodilation in the thoracic aorta of the diabetic OVX rats, which was partially attenuated by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methylester (L-NAME) and the GPR30-selective antagonist G15. Dose-dependent vasoconstrictive responses to phenylephrine were attenuated significantly in the rings of the thoracic aorta following the acute G1 administration in the diabetic OVX rats. This effect of G1 was abolished partially by L-NAME and G15. The acute administration of G1 increased significantly the eNOS activity and the concentration of NO in the endothelial cells exposed to high glucose. G1 treatment induced an enhanced endothelium-dependent relaxation to acetylcholine (Ach) in the diabetic OVX rats. Further examination revealed that G1 induced vasodilation in the diabetic OVX rats by increasing the phosphorylation of eNOS. These findings provide preliminary evidence that GPR30 activation leads to eNOS activation, as well as vasodilation, to a certain degree and has beneficial effects on vascular function in diabetic OVX rats.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22679517</pmid><doi>10.1371/journal.pone.0038787</doi><tpages>e38787</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylcholine Activation Animals Aorta Arginine Biology Blood Glucose - drug effects Body Weight - drug effects Cardiovascular system Diabetes mellitus Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - drug therapy Diabetes therapy Endothelial cells Endothelium Estrogens Female Glucose Hypoglycemic Agents - therapeutic use Insulin - blood Kinases Medicine Menopause NG-Nitroarginine methyl ester Nitric oxide Nitric Oxide - blood Nitric-oxide synthase Ovariectomy Phenylephrine Phosphorylation Rats Receptors, G-Protein-Coupled - agonists Rodents Thorax Type 2 diabetes Vasodilation Vasodilator agents |
| title | Improvement of vascular function by acute and chronic treatment with the GPR30 agonist G1 in experimental diabetes mellitus |
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