Nitric oxide release mediates vasodilator responses to endomorphin 1 but not nociceptin/OFQ in the hindquarters vascular bed of the rat
We have recently shown that endomorphin1, an endogenous ligand for the μ-opioid receptor, and nociceptin (Orphanin FQ; OFQ), an endogenous ligand for the ORL 1 receptor, have substantial vasodilator activity in the hindquarters vascular bed of the rat. In the present study, the role of nitric oxide,...
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| Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 1998, Vol.19 (9), p.1595-1602 |
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| creator | Champion, H.C Bivalacqua, T.J Friedman, D.E Zadina, J.E Kastin, A.J Kadowitz, P.J |
| description | We have recently shown that endomorphin1, an endogenous ligand for the μ-opioid receptor, and nociceptin (Orphanin FQ; OFQ), an endogenous ligand for the ORL
1 receptor, have substantial vasodilator activity in the hindquarters vascular bed of the rat. In the present study, the role of nitric oxide, vasodilator prostaglandins, and the opening of
K
+
ATP
channels in mediating vasodilator responses to endomorphin 1, PL017, and DAMGO was investigated in the regional vascular bed in the rat. Under constant-flow conditions, injections of the μ-selective agonists endomorphin 1, PL017 ([
N-MePhe
3,
d-Pro
4]-morphiceptin), and DAMGO, and the ORL
1 receptor agonist nociceptin/OFQ produced dose-dependent decreases in hindquarters perfusion pressure. Vasodilator responses to endomorphin 1, PL017, and DAMGO, and the endothelium-dependent vasodilators acetylcholine and adrenomedullin were attenuated by the nitric oxide synthase inhibitor
l-NAME (50 mg/kg IV) at a time when vasodilator responses to nociceptin/OFQ were not altered. Vasodilator responses to isoproterenol and prostaglandin E
1, agents known to increase cAMP levels, and the nitric oxide donor DEA/NO were not altered by the nitric oxide synthase inhibitor. Responses to endomorphin 1, PL017, DAMGO, and nociceptin/OFQ were not altered by sodium meclofenamate at a time when vasodilator responses to arachidonic acid were reduced significantly or after administration of U-37883A at a time when vasodilator responses to levcromakalim were reduced significantly. The results of these studies indicate that responses to endomorphin 1, PL017, and DAMGO are mediated in large part by the release of nitric oxide, while responses to nociceptin/OFQ are mediated by an
l-NAME-insensitive mechanism. Moreover, these results demonstrate that responses to these peptides are not mediated by the release of vasodilator prostaglandins or the opening of
K
+
ATP
channels the hindquarters vascular bed. |
| doi_str_mv | 10.1016/S0196-9781(98)00110-7 |
| format | Article |
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1 receptor, have substantial vasodilator activity in the hindquarters vascular bed of the rat. In the present study, the role of nitric oxide, vasodilator prostaglandins, and the opening of
K
+
ATP
channels in mediating vasodilator responses to endomorphin 1, PL017, and DAMGO was investigated in the regional vascular bed in the rat. Under constant-flow conditions, injections of the μ-selective agonists endomorphin 1, PL017 ([
N-MePhe
3,
d-Pro
4]-morphiceptin), and DAMGO, and the ORL
1 receptor agonist nociceptin/OFQ produced dose-dependent decreases in hindquarters perfusion pressure. Vasodilator responses to endomorphin 1, PL017, and DAMGO, and the endothelium-dependent vasodilators acetylcholine and adrenomedullin were attenuated by the nitric oxide synthase inhibitor
l-NAME (50 mg/kg IV) at a time when vasodilator responses to nociceptin/OFQ were not altered. Vasodilator responses to isoproterenol and prostaglandin E
1, agents known to increase cAMP levels, and the nitric oxide donor DEA/NO were not altered by the nitric oxide synthase inhibitor. Responses to endomorphin 1, PL017, DAMGO, and nociceptin/OFQ were not altered by sodium meclofenamate at a time when vasodilator responses to arachidonic acid were reduced significantly or after administration of U-37883A at a time when vasodilator responses to levcromakalim were reduced significantly. The results of these studies indicate that responses to endomorphin 1, PL017, and DAMGO are mediated in large part by the release of nitric oxide, while responses to nociceptin/OFQ are mediated by an
l-NAME-insensitive mechanism. Moreover, these results demonstrate that responses to these peptides are not mediated by the release of vasodilator prostaglandins or the opening of
K
+
ATP
channels the hindquarters vascular bed.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/S0196-9781(98)00110-7</identifier><identifier>PMID: 9864068</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adamantane - analogs & derivatives ; Adamantane - pharmacology ; Animals ; Blood Vessels - drug effects ; Endomorphin 1 ; Endorphins - pharmacology ; Endothelium, Vascular - metabolism ; Endothelium-dependent vasodilator ; Enkephalin, Ala-MePhe-Gly ; Enkephalins - pharmacology ; Hindquarters vascular bed ; Meclofenamic Acid - pharmacology ; Morpholines - pharmacology ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - metabolism ; Nitric oxide-dependent vasodilator ; Nociceptin ; Oligopeptides - pharmacology ; Opioid Peptides - pharmacology ; Potassium Channels - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid - agonists ; Regional Blood Flow - drug effects ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology</subject><ispartof>Peptides (New York, N.Y. : 1980), 1998, Vol.19 (9), p.1595-1602</ispartof><rights>1998 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-c36ff65faac284df277533497db5ac8de8cf4f7a4cb897ac461edb6e67eb0e573</citedby><cites>FETCH-LOGICAL-c360t-c36ff65faac284df277533497db5ac8de8cf4f7a4cb897ac461edb6e67eb0e573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0196-9781(98)00110-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9864068$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Champion, H.C</creatorcontrib><creatorcontrib>Bivalacqua, T.J</creatorcontrib><creatorcontrib>Friedman, D.E</creatorcontrib><creatorcontrib>Zadina, J.E</creatorcontrib><creatorcontrib>Kastin, A.J</creatorcontrib><creatorcontrib>Kadowitz, P.J</creatorcontrib><title>Nitric oxide release mediates vasodilator responses to endomorphin 1 but not nociceptin/OFQ in the hindquarters vascular bed of the rat</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>We have recently shown that endomorphin1, an endogenous ligand for the μ-opioid receptor, and nociceptin (Orphanin FQ; OFQ), an endogenous ligand for the ORL
1 receptor, have substantial vasodilator activity in the hindquarters vascular bed of the rat. In the present study, the role of nitric oxide, vasodilator prostaglandins, and the opening of
K
+
ATP
channels in mediating vasodilator responses to endomorphin 1, PL017, and DAMGO was investigated in the regional vascular bed in the rat. Under constant-flow conditions, injections of the μ-selective agonists endomorphin 1, PL017 ([
N-MePhe
3,
d-Pro
4]-morphiceptin), and DAMGO, and the ORL
1 receptor agonist nociceptin/OFQ produced dose-dependent decreases in hindquarters perfusion pressure. Vasodilator responses to endomorphin 1, PL017, and DAMGO, and the endothelium-dependent vasodilators acetylcholine and adrenomedullin were attenuated by the nitric oxide synthase inhibitor
l-NAME (50 mg/kg IV) at a time when vasodilator responses to nociceptin/OFQ were not altered. Vasodilator responses to isoproterenol and prostaglandin E
1, agents known to increase cAMP levels, and the nitric oxide donor DEA/NO were not altered by the nitric oxide synthase inhibitor. Responses to endomorphin 1, PL017, DAMGO, and nociceptin/OFQ were not altered by sodium meclofenamate at a time when vasodilator responses to arachidonic acid were reduced significantly or after administration of U-37883A at a time when vasodilator responses to levcromakalim were reduced significantly. The results of these studies indicate that responses to endomorphin 1, PL017, and DAMGO are mediated in large part by the release of nitric oxide, while responses to nociceptin/OFQ are mediated by an
l-NAME-insensitive mechanism. Moreover, these results demonstrate that responses to these peptides are not mediated by the release of vasodilator prostaglandins or the opening of
K
+
ATP
channels the hindquarters vascular bed.</description><subject>Adamantane - analogs & derivatives</subject><subject>Adamantane - pharmacology</subject><subject>Animals</subject><subject>Blood Vessels - drug effects</subject><subject>Endomorphin 1</subject><subject>Endorphins - pharmacology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium-dependent vasodilator</subject><subject>Enkephalin, Ala-MePhe-Gly</subject><subject>Enkephalins - pharmacology</subject><subject>Hindquarters vascular bed</subject><subject>Meclofenamic Acid - pharmacology</subject><subject>Morpholines - pharmacology</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric oxide-dependent vasodilator</subject><subject>Nociceptin</subject><subject>Oligopeptides - pharmacology</subject><subject>Opioid Peptides - pharmacology</subject><subject>Potassium Channels - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Opioid - agonists</subject><subject>Regional Blood Flow - drug effects</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd9qHCEYxSU0pNtNHyHgVWkvptGdGf9clRK6bWBJCEmvxdFPYpgdJ-qE9Any2nV2l73NhQqen9_BcxC6oOQ7JZRd3hMqWSW5oF-l-EYIpaTiJ2hBBa-rljL5AS2OyEf0KaUnQkjTSHGGzqRgDWFigd5ufI7e4PDqLeAIPegEeAvW6wwJv-gUrO91DrGIaQxDKrc5YBhs2IY4PvoBU9xNGQ9hXsYbGLMfLm_Xd7ho-RFwYezzpGOGuJtopl5H3IHFwe2AqPM5OnW6T_D5cC7R3_Wvh6s_1eb29_XVz01lakbyvDvHWqe1WYnGuhXnbV03ktuu1UZYEMY1juvGdEJybRpGwXYMGIeOQMvrJfqynzvG8DxBymrrk4G-1wOEKSkmKVkRKgrY7kETQ0oRnBqj3-r4T1Gi5gLUrgA1p6ukULsC1GxwcTCYuhLj8dUh8aL_2OtQfvniIapkPAymJB7BZGWDf8fhPwptmPg</recordid><startdate>1998</startdate><enddate>1998</enddate><creator>Champion, H.C</creator><creator>Bivalacqua, T.J</creator><creator>Friedman, D.E</creator><creator>Zadina, J.E</creator><creator>Kastin, A.J</creator><creator>Kadowitz, P.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>1998</creationdate><title>Nitric oxide release mediates vasodilator responses to endomorphin 1 but not nociceptin/OFQ in the hindquarters vascular bed of the rat</title><author>Champion, H.C ; Bivalacqua, T.J ; Friedman, D.E ; Zadina, J.E ; Kastin, A.J ; Kadowitz, P.J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c360t-c36ff65faac284df277533497db5ac8de8cf4f7a4cb897ac461edb6e67eb0e573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adamantane - analogs & derivatives</topic><topic>Adamantane - pharmacology</topic><topic>Animals</topic><topic>Blood Vessels - drug effects</topic><topic>Endomorphin 1</topic><topic>Endorphins - pharmacology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium-dependent vasodilator</topic><topic>Enkephalin, Ala-MePhe-Gly</topic><topic>Enkephalins - pharmacology</topic><topic>Hindquarters vascular bed</topic><topic>Meclofenamic Acid - pharmacology</topic><topic>Morpholines - pharmacology</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric oxide-dependent vasodilator</topic><topic>Nociceptin</topic><topic>Oligopeptides - pharmacology</topic><topic>Opioid Peptides - pharmacology</topic><topic>Potassium Channels - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Opioid - agonists</topic><topic>Regional Blood Flow - drug effects</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Champion, H.C</creatorcontrib><creatorcontrib>Bivalacqua, T.J</creatorcontrib><creatorcontrib>Friedman, D.E</creatorcontrib><creatorcontrib>Zadina, J.E</creatorcontrib><creatorcontrib>Kastin, A.J</creatorcontrib><creatorcontrib>Kadowitz, P.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>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Champion, H.C</au><au>Bivalacqua, T.J</au><au>Friedman, D.E</au><au>Zadina, J.E</au><au>Kastin, A.J</au><au>Kadowitz, P.J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric oxide release mediates vasodilator responses to endomorphin 1 but not nociceptin/OFQ in the hindquarters vascular bed of the rat</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>1998</date><risdate>1998</risdate><volume>19</volume><issue>9</issue><spage>1595</spage><epage>1602</epage><pages>1595-1602</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><abstract>We have recently shown that endomorphin1, an endogenous ligand for the μ-opioid receptor, and nociceptin (Orphanin FQ; OFQ), an endogenous ligand for the ORL
1 receptor, have substantial vasodilator activity in the hindquarters vascular bed of the rat. In the present study, the role of nitric oxide, vasodilator prostaglandins, and the opening of
K
+
ATP
channels in mediating vasodilator responses to endomorphin 1, PL017, and DAMGO was investigated in the regional vascular bed in the rat. Under constant-flow conditions, injections of the μ-selective agonists endomorphin 1, PL017 ([
N-MePhe
3,
d-Pro
4]-morphiceptin), and DAMGO, and the ORL
1 receptor agonist nociceptin/OFQ produced dose-dependent decreases in hindquarters perfusion pressure. Vasodilator responses to endomorphin 1, PL017, and DAMGO, and the endothelium-dependent vasodilators acetylcholine and adrenomedullin were attenuated by the nitric oxide synthase inhibitor
l-NAME (50 mg/kg IV) at a time when vasodilator responses to nociceptin/OFQ were not altered. Vasodilator responses to isoproterenol and prostaglandin E
1, agents known to increase cAMP levels, and the nitric oxide donor DEA/NO were not altered by the nitric oxide synthase inhibitor. Responses to endomorphin 1, PL017, DAMGO, and nociceptin/OFQ were not altered by sodium meclofenamate at a time when vasodilator responses to arachidonic acid were reduced significantly or after administration of U-37883A at a time when vasodilator responses to levcromakalim were reduced significantly. The results of these studies indicate that responses to endomorphin 1, PL017, and DAMGO are mediated in large part by the release of nitric oxide, while responses to nociceptin/OFQ are mediated by an
l-NAME-insensitive mechanism. Moreover, these results demonstrate that responses to these peptides are not mediated by the release of vasodilator prostaglandins or the opening of
K
+
ATP
channels the hindquarters vascular bed.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>9864068</pmid><doi>10.1016/S0196-9781(98)00110-7</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0196-9781 |
| ispartof | Peptides (New York, N.Y. : 1980), 1998, Vol.19 (9), p.1595-1602 |
| issn | 0196-9781 1873-5169 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69102018 |
| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Adamantane - analogs & derivatives Adamantane - pharmacology Animals Blood Vessels - drug effects Endomorphin 1 Endorphins - pharmacology Endothelium, Vascular - metabolism Endothelium-dependent vasodilator Enkephalin, Ala-MePhe-Gly Enkephalins - pharmacology Hindquarters vascular bed Meclofenamic Acid - pharmacology Morpholines - pharmacology NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - metabolism Nitric oxide-dependent vasodilator Nociceptin Oligopeptides - pharmacology Opioid Peptides - pharmacology Potassium Channels - metabolism Rats Rats, Sprague-Dawley Receptors, Opioid - agonists Regional Blood Flow - drug effects Vasodilation - drug effects Vasodilator Agents - pharmacology |
| title | Nitric oxide release mediates vasodilator responses to endomorphin 1 but not nociceptin/OFQ in the hindquarters vascular bed of the rat |
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