Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries
OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy. STUDY DESIGN: The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-preg...
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| Veröffentlicht in: | American journal of obstetrics and gynecology 1997-04, Vol.176 (4), p.856-864 |
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| creator | Ni, Yajun Meyer, Marjorie Osol, George |
| description | OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy.
STUDY DESIGN: The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-pregnant rats (day 19 to 20) versus age-matched nonpregnant controls. The effects of nitric oxide synthase inhibition (Nω-nitro-
l-arginine) on arterial tone and reactivity under basal and activated (phenylephrine) conditions were determined, as was arterial reactivity to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter.
RESULTS: (1) Maximal constriction to Nω-nitro-
l-arginine was significantly enhanced under basal (nonstimulated) conditions in arteries from late-pregnant versus nonpregnant rats (changes in lumen diameter 37% ± 8% vs 9.3 ± 6.2%, respectively,
p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L Nω-nitro-
l-arginine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 ± 23 nmol/L vs 33 ± 8 nmol/L, control vs treated vessels,
p < 0.05) but was without statistically significant effect on arteries from nonpregnant animals (control 255 ± 164 nmol/L, treated 250 ± 102 nmol/L,
p > 0.05). (3) The threshold concentration of acetylcholine required to elicit endothelium-dependent dilation was significantly lower in late-pregnant versus nonpregnant arteries (1.4 ± 0.2 nmol/L vs 12.2 ± 3.8 nmol/L,
p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenous nitrodilator (sodium nitroprusside) was identical in late-pregnant versus nonpregnant vessels.
CONCLUSION: Endothelial vasodilator influences are augmented during pregnancy under basal, activated (phenylephrine), and chemically provoked (acetylcholine) conditions in uterine arteries by enhanced release of nitric oxide. (Am J Obstet Gynecol 1997;176:856-64.) |
| doi_str_mv | 10.1016/S0002-9378(97)70611-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78967895</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0002937897706112</els_id><sourcerecordid>78967895</sourcerecordid><originalsourceid>FETCH-LOGICAL-c507t-c10b3099a783f45ffe1ed19692de6b644128a13c316c930a152016d9640848453</originalsourceid><addsrcrecordid>eNqFkNFKwzAUhoMoc04fYdALEb2oJmmbJlciQ6cwUFCvQ5acQqRrZ5INvfMdfEOfxHSru_UiJOF8f07Oh9CY4EuCCbt6xhjTVGQlPxflRYkZISndQ0OCRZkyzvg-Gu6QQ3Tk_Vt3pYIO0EAQWsTAED1NwQcVbNskttEOlAefNDY4q5P2wxr4-fpegLEqgEnWyrfG1n944lRIVgGcbSBRrjuAP0YHlao9nPT7CL3e3b5M7tPZ4_RhcjNLdYHLkGqC5xkWQpU8q_KiqoCAIYIJaoDNWZ4TyhXJdEaYFhlWpKBxaCNYjnnO8yIbobPtu0vXvq_iEHJhvYa6Vg20Ky9LLlhcHVhsQe1a7x1UcunsQrlPSbDsTMqNSdlpkqKUG5OSxty4b7CaRwO7VK8u1k_7uvJa1ZVTjbZ-h1FWEMy79tdbDKKMtQUnvbbQ6OjUgQ7StPafj_wCT0mQEA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>78967895</pqid></control><display><type>article</type><title>Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Ni, Yajun ; Meyer, Marjorie ; Osol, George</creator><creatorcontrib>Ni, Yajun ; Meyer, Marjorie ; Osol, George</creatorcontrib><description>OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy.
STUDY DESIGN: The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-pregnant rats (day 19 to 20) versus age-matched nonpregnant controls. The effects of nitric oxide synthase inhibition (Nω-nitro-
l-arginine) on arterial tone and reactivity under basal and activated (phenylephrine) conditions were determined, as was arterial reactivity to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter.
RESULTS: (1) Maximal constriction to Nω-nitro-
l-arginine was significantly enhanced under basal (nonstimulated) conditions in arteries from late-pregnant versus nonpregnant rats (changes in lumen diameter 37% ± 8% vs 9.3 ± 6.2%, respectively,
p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L Nω-nitro-
l-arginine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 ± 23 nmol/L vs 33 ± 8 nmol/L, control vs treated vessels,
p < 0.05) but was without statistically significant effect on arteries from nonpregnant animals (control 255 ± 164 nmol/L, treated 250 ± 102 nmol/L,
p > 0.05). (3) The threshold concentration of acetylcholine required to elicit endothelium-dependent dilation was significantly lower in late-pregnant versus nonpregnant arteries (1.4 ± 0.2 nmol/L vs 12.2 ± 3.8 nmol/L,
p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenous nitrodilator (sodium nitroprusside) was identical in late-pregnant versus nonpregnant vessels.
CONCLUSION: Endothelial vasodilator influences are augmented during pregnancy under basal, activated (phenylephrine), and chemically provoked (acetylcholine) conditions in uterine arteries by enhanced release of nitric oxide. (Am J Obstet Gynecol 1997;176:856-64.)</description><identifier>ISSN: 0002-9378</identifier><identifier>EISSN: 1097-6868</identifier><identifier>DOI: 10.1016/S0002-9378(97)70611-2</identifier><identifier>PMID: 9125611</identifier><identifier>CODEN: AJOGAH</identifier><language>eng</language><publisher>Philadelphia, PA: Mosby, Inc</publisher><subject>Acetylcholine - pharmacology ; Animals ; Arteries - drug effects ; Arteries - physiology ; Biological and medical sciences ; endothelium ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Enzyme Inhibitors - pharmacology ; Female ; Fundamental and applied biological sciences. Psychology ; Mother. Fetoplacental unit. Mammary gland. Milk ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; nitric oxide ; Nitric Oxide - blood ; Nitric Oxide - physiology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitroarginine - pharmacology ; Nitroprusside - pharmacology ; Phenylephrine - pharmacology ; Pregnancy ; Pregnancy, Animal - physiology ; Pregnancy. Parturition. Lactation ; Rats ; Rats, Sprague-Dawley ; uterine arteries ; Uterus - blood supply ; Vasoconstrictor Agents - pharmacology ; Vasodilation - drug effects ; Vasodilation - physiology ; Vasodilator Agents - pharmacology ; Vertebrates: reproduction</subject><ispartof>American journal of obstetrics and gynecology, 1997-04, Vol.176 (4), p.856-864</ispartof><rights>1997 Mosby, Inc.</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-c10b3099a783f45ffe1ed19692de6b644128a13c316c930a152016d9640848453</citedby><cites>FETCH-LOGICAL-c507t-c10b3099a783f45ffe1ed19692de6b644128a13c316c930a152016d9640848453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0002-9378(97)70611-2$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,3550,23930,23931,25140,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2651085$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9125611$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ni, Yajun</creatorcontrib><creatorcontrib>Meyer, Marjorie</creatorcontrib><creatorcontrib>Osol, George</creatorcontrib><title>Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries</title><title>American journal of obstetrics and gynecology</title><addtitle>Am J Obstet Gynecol</addtitle><description>OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy.
STUDY DESIGN: The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-pregnant rats (day 19 to 20) versus age-matched nonpregnant controls. The effects of nitric oxide synthase inhibition (Nω-nitro-
l-arginine) on arterial tone and reactivity under basal and activated (phenylephrine) conditions were determined, as was arterial reactivity to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter.
RESULTS: (1) Maximal constriction to Nω-nitro-
l-arginine was significantly enhanced under basal (nonstimulated) conditions in arteries from late-pregnant versus nonpregnant rats (changes in lumen diameter 37% ± 8% vs 9.3 ± 6.2%, respectively,
p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L Nω-nitro-
l-arginine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 ± 23 nmol/L vs 33 ± 8 nmol/L, control vs treated vessels,
p < 0.05) but was without statistically significant effect on arteries from nonpregnant animals (control 255 ± 164 nmol/L, treated 250 ± 102 nmol/L,
p > 0.05). (3) The threshold concentration of acetylcholine required to elicit endothelium-dependent dilation was significantly lower in late-pregnant versus nonpregnant arteries (1.4 ± 0.2 nmol/L vs 12.2 ± 3.8 nmol/L,
p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenous nitrodilator (sodium nitroprusside) was identical in late-pregnant versus nonpregnant vessels.
CONCLUSION: Endothelial vasodilator influences are augmented during pregnancy under basal, activated (phenylephrine), and chemically provoked (acetylcholine) conditions in uterine arteries by enhanced release of nitric oxide. (Am J Obstet Gynecol 1997;176:856-64.)</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Arteries - drug effects</subject><subject>Arteries - physiology</subject><subject>Biological and medical sciences</subject><subject>endothelium</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Mother. Fetoplacental unit. Mammary gland. Milk</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>nitric oxide</subject><subject>Nitric Oxide - blood</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitroarginine - pharmacology</subject><subject>Nitroprusside - pharmacology</subject><subject>Phenylephrine - pharmacology</subject><subject>Pregnancy</subject><subject>Pregnancy, Animal - physiology</subject><subject>Pregnancy. Parturition. Lactation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>uterine arteries</subject><subject>Uterus - blood supply</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vertebrates: reproduction</subject><issn>0002-9378</issn><issn>1097-6868</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkNFKwzAUhoMoc04fYdALEb2oJmmbJlciQ6cwUFCvQ5acQqRrZ5INvfMdfEOfxHSru_UiJOF8f07Oh9CY4EuCCbt6xhjTVGQlPxflRYkZISndQ0OCRZkyzvg-Gu6QQ3Tk_Vt3pYIO0EAQWsTAED1NwQcVbNskttEOlAefNDY4q5P2wxr4-fpegLEqgEnWyrfG1n944lRIVgGcbSBRrjuAP0YHlao9nPT7CL3e3b5M7tPZ4_RhcjNLdYHLkGqC5xkWQpU8q_KiqoCAIYIJaoDNWZ4TyhXJdEaYFhlWpKBxaCNYjnnO8yIbobPtu0vXvq_iEHJhvYa6Vg20Ky9LLlhcHVhsQe1a7x1UcunsQrlPSbDsTMqNSdlpkqKUG5OSxty4b7CaRwO7VK8u1k_7uvJa1ZVTjbZ-h1FWEMy79tdbDKKMtQUnvbbQ6OjUgQ7StPafj_wCT0mQEA</recordid><startdate>19970401</startdate><enddate>19970401</enddate><creator>Ni, Yajun</creator><creator>Meyer, Marjorie</creator><creator>Osol, George</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><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>19970401</creationdate><title>Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries</title><author>Ni, Yajun ; Meyer, Marjorie ; Osol, George</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-c10b3099a783f45ffe1ed19692de6b644128a13c316c930a152016d9640848453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Arteries - drug effects</topic><topic>Arteries - physiology</topic><topic>Biological and medical sciences</topic><topic>endothelium</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Mother. Fetoplacental unit. Mammary gland. Milk</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>nitric oxide</topic><topic>Nitric Oxide - blood</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitroarginine - pharmacology</topic><topic>Nitroprusside - pharmacology</topic><topic>Phenylephrine - pharmacology</topic><topic>Pregnancy</topic><topic>Pregnancy, Animal - physiology</topic><topic>Pregnancy. Parturition. Lactation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>uterine arteries</topic><topic>Uterus - blood supply</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ni, Yajun</creatorcontrib><creatorcontrib>Meyer, Marjorie</creatorcontrib><creatorcontrib>Osol, George</creatorcontrib><collection>Pascal-Francis</collection><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>American journal of obstetrics and gynecology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ni, Yajun</au><au>Meyer, Marjorie</au><au>Osol, George</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries</atitle><jtitle>American journal of obstetrics and gynecology</jtitle><addtitle>Am J Obstet Gynecol</addtitle><date>1997-04-01</date><risdate>1997</risdate><volume>176</volume><issue>4</issue><spage>856</spage><epage>864</epage><pages>856-864</pages><issn>0002-9378</issn><eissn>1097-6868</eissn><coden>AJOGAH</coden><abstract>OBJECTIVE: The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy.
STUDY DESIGN: The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-pregnant rats (day 19 to 20) versus age-matched nonpregnant controls. The effects of nitric oxide synthase inhibition (Nω-nitro-
l-arginine) on arterial tone and reactivity under basal and activated (phenylephrine) conditions were determined, as was arterial reactivity to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter.
RESULTS: (1) Maximal constriction to Nω-nitro-
l-arginine was significantly enhanced under basal (nonstimulated) conditions in arteries from late-pregnant versus nonpregnant rats (changes in lumen diameter 37% ± 8% vs 9.3 ± 6.2%, respectively,
p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L Nω-nitro-
l-arginine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 ± 23 nmol/L vs 33 ± 8 nmol/L, control vs treated vessels,
p < 0.05) but was without statistically significant effect on arteries from nonpregnant animals (control 255 ± 164 nmol/L, treated 250 ± 102 nmol/L,
p > 0.05). (3) The threshold concentration of acetylcholine required to elicit endothelium-dependent dilation was significantly lower in late-pregnant versus nonpregnant arteries (1.4 ± 0.2 nmol/L vs 12.2 ± 3.8 nmol/L,
p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenous nitrodilator (sodium nitroprusside) was identical in late-pregnant versus nonpregnant vessels.
CONCLUSION: Endothelial vasodilator influences are augmented during pregnancy under basal, activated (phenylephrine), and chemically provoked (acetylcholine) conditions in uterine arteries by enhanced release of nitric oxide. (Am J Obstet Gynecol 1997;176:856-64.)</abstract><cop>Philadelphia, PA</cop><pub>Mosby, Inc</pub><pmid>9125611</pmid><doi>10.1016/S0002-9378(97)70611-2</doi><tpages>9</tpages></addata></record> |
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| ispartof | American journal of obstetrics and gynecology, 1997-04, Vol.176 (4), p.856-864 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Acetylcholine - pharmacology Animals Arteries - drug effects Arteries - physiology Biological and medical sciences endothelium Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Enzyme Inhibitors - pharmacology Female Fundamental and applied biological sciences. Psychology Mother. Fetoplacental unit. Mammary gland. Milk Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology nitric oxide Nitric Oxide - blood Nitric Oxide - physiology Nitric Oxide Synthase - antagonists & inhibitors Nitroarginine - pharmacology Nitroprusside - pharmacology Phenylephrine - pharmacology Pregnancy Pregnancy, Animal - physiology Pregnancy. Parturition. Lactation Rats Rats, Sprague-Dawley uterine arteries Uterus - blood supply Vasoconstrictor Agents - pharmacology Vasodilation - drug effects Vasodilation - physiology Vasodilator Agents - pharmacology Vertebrates: reproduction |
| title | Gestation increases nitric oxide–mediated vasodilation in rat uterine arteries |
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