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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Veröffentlicht in:American journal of hypertension 2001, Vol.14 (1), p.77-83
Hauptverfasser: Nishikawa, Satoshi, Miyamoto, Atsushi, Yamamoto, Hiroyuki, Ohshika, Hideyo, Kudo, Ryuichi
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container_end_page 83
container_issue 1
container_start_page 77
container_title American journal of hypertension
container_volume 14
creator Nishikawa, Satoshi
Miyamoto, Atsushi
Yamamoto, Hiroyuki
Ohshika, Hideyo
Kudo, Ryuichi
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.
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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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source Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection
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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