Preeclamptic serum enhances endothelin-converting enzyme expression in cultured endothelial cells
Increased vascular sensitivity to vasoconstrictors, such as angiotensin II and epinephrine, is observed in preeclampsia (PE). Recently, it was suggested that abnormal endothelial function might contribute to the pathophysiologic changes in PE. We investigated vasoconstrictor (angiotensin II and epin...
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description | Increased vascular sensitivity to vasoconstrictors, such as angiotensin II and epinephrine, is observed in preeclampsia (PE). Recently, it was suggested that abnormal endothelial function might contribute to the pathophysiologic changes in PE. We investigated vasoconstrictor (angiotensin II and epinephrine)-induced endothelin-1 (ET-1) release from human umbilical vein endothelial cells incubated with sera from women with PE compared with normotensive pregnant and nonpregnant women. Moreover, inositol 1,4,5-trisphosphate production and endothelin-converting enzyme (ECE) expression in human umbilical vein endothelial cells were also evaluated. There were no significant differences in ET-1 release without vasoconstrictors among the three groups (nonpregnant, normotensive pregnant, and PE). No significant differences in basal inositol 1,4,5-trisphosphate production and ECE expression without vasoconstrictors were detected among the three groups. Vasoconstrictor-induced ET-1 release was significantly increased by PE sera. No significant difference was detected in vasoconstrictor-induced inositol 1,4,5-trisphosphate production among the three groups. However, ECE expression after incubation with vasoconstrictor was significantly increased by PE sera. Our results suggest that ET-1 release from endothelial cells may contribute to the increased vascular sensitivity to vasoconstrictors observed in PE, and that vasoconstrictor-induced ET-1 release may be related to enhanced ECE expression. |
doi_str_mv | 10.1016/S0895-7061(00)01244-9 |
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Recently, it was suggested that abnormal endothelial function might contribute to the pathophysiologic changes in PE. We investigated vasoconstrictor (angiotensin II and epinephrine)-induced endothelin-1 (ET-1) release from human umbilical vein endothelial cells incubated with sera from women with PE compared with normotensive pregnant and nonpregnant women. Moreover, inositol 1,4,5-trisphosphate production and endothelin-converting enzyme (ECE) expression in human umbilical vein endothelial cells were also evaluated. There were no significant differences in ET-1 release without vasoconstrictors among the three groups (nonpregnant, normotensive pregnant, and PE). No significant differences in basal inositol 1,4,5-trisphosphate production and ECE expression without vasoconstrictors were detected among the three groups. Vasoconstrictor-induced ET-1 release was significantly increased by PE sera. No significant difference was detected in vasoconstrictor-induced inositol 1,4,5-trisphosphate production among the three groups. However, ECE expression after incubation with vasoconstrictor was significantly increased by PE sera. Our results suggest that ET-1 release from endothelial cells may contribute to the increased vascular sensitivity to vasoconstrictors observed in PE, and that vasoconstrictor-induced ET-1 release may be related to enhanced ECE expression.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/S0895-7061(00)01244-9</identifier><identifier>PMID: 11206686</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Angiotensin II - pharmacology ; Aspartic Acid Endopeptidases - metabolism ; Biological and medical sciences ; Blood Physiological Phenomena ; Cells, Cultured ; Diseases of mother, fetus and pregnancy ; endothelin-1 ; Endothelin-1 - metabolism ; endothelin-converting enzyme ; Endothelin-Converting Enzymes ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Epinephrine - pharmacology ; Female ; Gynecology. Andrology. Obstetrics ; human umbilical vein endothelial cells ; Humans ; Inositol 1,4,5-Trisphosphate - biosynthesis ; Medical sciences ; Metalloendopeptidases ; Pre-Eclampsia - blood ; Preeclampsia ; Pregnancy ; Pregnancy. Fetus. Placenta ; Reference Values ; Vasoconstrictor Agents - pharmacology</subject><ispartof>American journal of hypertension, 2001, Vol.14 (1), p.77-83</ispartof><rights>2001 American Journal of Hypertension, Ltd.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-8ca7127e9f6b03de3e5aaac6dc5dcd0ccb8d9e416b920b87fd84ee143eff4a93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=866127$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11206686$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishikawa, Satoshi</creatorcontrib><creatorcontrib>Miyamoto, Atsushi</creatorcontrib><creatorcontrib>Yamamoto, Hiroyuki</creatorcontrib><creatorcontrib>Ohshika, Hideyo</creatorcontrib><creatorcontrib>Kudo, Ryuichi</creatorcontrib><title>Preeclamptic serum enhances endothelin-converting enzyme expression in cultured endothelial cells</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Increased vascular sensitivity to vasoconstrictors, such as angiotensin II and epinephrine, is observed in preeclampsia (PE). Recently, it was suggested that abnormal endothelial function might contribute to the pathophysiologic changes in PE. We investigated vasoconstrictor (angiotensin II and epinephrine)-induced endothelin-1 (ET-1) release from human umbilical vein endothelial cells incubated with sera from women with PE compared with normotensive pregnant and nonpregnant women. Moreover, inositol 1,4,5-trisphosphate production and endothelin-converting enzyme (ECE) expression in human umbilical vein endothelial cells were also evaluated. There were no significant differences in ET-1 release without vasoconstrictors among the three groups (nonpregnant, normotensive pregnant, and PE). No significant differences in basal inositol 1,4,5-trisphosphate production and ECE expression without vasoconstrictors were detected among the three groups. Vasoconstrictor-induced ET-1 release was significantly increased by PE sera. No significant difference was detected in vasoconstrictor-induced inositol 1,4,5-trisphosphate production among the three groups. However, ECE expression after incubation with vasoconstrictor was significantly increased by PE sera. Our results suggest that ET-1 release from endothelial cells may contribute to the increased vascular sensitivity to vasoconstrictors observed in PE, and that vasoconstrictor-induced ET-1 release may be related to enhanced ECE expression.</description><subject>Adult</subject><subject>Angiotensin II - pharmacology</subject><subject>Aspartic Acid Endopeptidases - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood Physiological Phenomena</subject><subject>Cells, Cultured</subject><subject>Diseases of mother, fetus and pregnancy</subject><subject>endothelin-1</subject><subject>Endothelin-1 - metabolism</subject><subject>endothelin-converting enzyme</subject><subject>Endothelin-Converting Enzymes</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Epinephrine - pharmacology</subject><subject>Female</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>human umbilical vein endothelial cells</subject><subject>Humans</subject><subject>Inositol 1,4,5-Trisphosphate - biosynthesis</subject><subject>Medical sciences</subject><subject>Metalloendopeptidases</subject><subject>Pre-Eclampsia - blood</subject><subject>Preeclampsia</subject><subject>Pregnancy</subject><subject>Pregnancy. Fetus. 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Andrology. Obstetrics</topic><topic>human umbilical vein endothelial cells</topic><topic>Humans</topic><topic>Inositol 1,4,5-Trisphosphate - biosynthesis</topic><topic>Medical sciences</topic><topic>Metalloendopeptidases</topic><topic>Pre-Eclampsia - blood</topic><topic>Preeclampsia</topic><topic>Pregnancy</topic><topic>Pregnancy. Fetus. Placenta</topic><topic>Reference Values</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishikawa, Satoshi</creatorcontrib><creatorcontrib>Miyamoto, Atsushi</creatorcontrib><creatorcontrib>Yamamoto, Hiroyuki</creatorcontrib><creatorcontrib>Ohshika, Hideyo</creatorcontrib><creatorcontrib>Kudo, Ryuichi</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishikawa, Satoshi</au><au>Miyamoto, Atsushi</au><au>Yamamoto, Hiroyuki</au><au>Ohshika, Hideyo</au><au>Kudo, Ryuichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preeclamptic serum enhances endothelin-converting enzyme expression in cultured endothelial cells</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2001</date><risdate>2001</risdate><volume>14</volume><issue>1</issue><spage>77</spage><epage>83</epage><pages>77-83</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>Increased vascular sensitivity to vasoconstrictors, such as angiotensin II and epinephrine, is observed in preeclampsia (PE). Recently, it was suggested that abnormal endothelial function might contribute to the pathophysiologic changes in PE. We investigated vasoconstrictor (angiotensin II and epinephrine)-induced endothelin-1 (ET-1) release from human umbilical vein endothelial cells incubated with sera from women with PE compared with normotensive pregnant and nonpregnant women. Moreover, inositol 1,4,5-trisphosphate production and endothelin-converting enzyme (ECE) expression in human umbilical vein endothelial cells were also evaluated. There were no significant differences in ET-1 release without vasoconstrictors among the three groups (nonpregnant, normotensive pregnant, and PE). No significant differences in basal inositol 1,4,5-trisphosphate production and ECE expression without vasoconstrictors were detected among the three groups. Vasoconstrictor-induced ET-1 release was significantly increased by PE sera. No significant difference was detected in vasoconstrictor-induced inositol 1,4,5-trisphosphate production among the three groups. However, ECE expression after incubation with vasoconstrictor was significantly increased by PE sera. Our results suggest that ET-1 release from endothelial cells may contribute to the increased vascular sensitivity to vasoconstrictors observed in PE, and that vasoconstrictor-induced ET-1 release may be related to enhanced ECE expression.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11206686</pmid><doi>10.1016/S0895-7061(00)01244-9</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Angiotensin II - pharmacology Aspartic Acid Endopeptidases - metabolism Biological and medical sciences Blood Physiological Phenomena Cells, Cultured Diseases of mother, fetus and pregnancy endothelin-1 Endothelin-1 - metabolism endothelin-converting enzyme Endothelin-Converting Enzymes Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Epinephrine - pharmacology Female Gynecology. Andrology. Obstetrics human umbilical vein endothelial cells Humans Inositol 1,4,5-Trisphosphate - biosynthesis Medical sciences Metalloendopeptidases Pre-Eclampsia - blood Preeclampsia Pregnancy Pregnancy. Fetus. Placenta Reference Values Vasoconstrictor Agents - pharmacology |
title | Preeclamptic serum enhances endothelin-converting enzyme expression in cultured endothelial cells |
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