Document Detail

Mechanisms underlying the reduced endothelium-dependent relaxation in human omental resistance artery in pre-eclampsia.
MedLine Citation:
PMID:  10944179     Owner:  NLM     Status:  MEDLINE    
1. In pre-eclampsia, a functional change occurs in the role played by endothelium-derived nitric oxide (NO) in the regulation of smooth muscle contraction in resistance arteries. We investigated the underlying mechanism in human omental resistance arteries from normotensive pregnant and pre-eclamptic women in the presence of diclofenac (an inhibitor of cyclo-oxygenase). 2. In endothelium-intact strips, the sensitivity to 9,11-epithio-11,12-methano-thromboxane A2 (STA2) was significantly higher in pre-eclampsia, and this was not modified by either NG-nitro-L-arginine (L-NNA, an inhibitor of NO synthase) or removal of the endothelium. 3. Bradykinin and substance P each produced an endothelium-dependent relaxation of the STA2-induced contraction in both groups, although the relaxation was significantly smaller for pre-eclampsia. L-NNA markedly attenuated the endothelium-dependent relaxation in the normotensive pregnant group but not in the pre-eclamptic group. 4. In the presence of L-NNA, the relaxation induced by sodium nitroprusside (SNP) on the STA2 contraction was significantly smaller for pre-eclamptic than for normotensive pregnant women. 5. In endothelium-denuded strips, the relaxation induced by 8-para-chlorophenyl thio-guanosine-3', 5'-cyclic monophosphate (8-pCPT-cGMP) on the STA2 contraction was significantly less for pre-eclampsia. 6. In beta-escin-skinned strips from both groups of women, 8-pCPT-cGMP (1-10 microM) concentration-dependently attenuated the contraction induced by 0.5 microM Ca2+. However, its relaxing action was significantly weaker in pre-eclampsia. 7. It is suggested that the weaker responsivene to NO seen in strips from pre-eclamptic women may be partly due to a reduced smooth muscle responsiveness to cyclic GMP.
Y Suzuki; J Kajikuri; K Suzumori; T Itoh
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of physiology     Volume:  527 Pt 1     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-10-05     Completed Date:  2000-11-07     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  163-74     Citation Subset:  IM    
Departments of Obstetrics and Gynecology and Pharmacology, Nagoya City University Medical School, Nagoya 467-8601, Japan.
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MeSH Terms
Benzimidazoles / pharmacology
Bradykinin / pharmacology
Calcium / metabolism
Calcium Channel Agonists / pharmacology
Cyclic GMP / analogs & derivatives,  physiology*
Cyclooxygenase Inhibitors / pharmacology
Endothelium, Vascular / drug effects,  physiology*
Mesenteric Arteries / drug effects,  physiology*
Muscle Contraction / drug effects,  physiology*
Muscle, Smooth / drug effects,  physiology*
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Nitroprusside / pharmacology
Omentum / blood supply*,  physiology
Potassium / metabolism
Pre-Eclampsia / physiopathology*
Substance P / pharmacology
Thromboxane A2 / analogs & derivatives*,  pharmacology
Vasodilation / drug effects,  physiology*
Reg. No./Substance:
0/Benzimidazoles; 0/Calcium Channel Agonists; 0/Cyclooxygenase Inhibitors; 10045-45-1/1-ethyl-2-benzimidazolinone; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 33507-63-0/Substance P; 57576-52-0/Thromboxane A2; 58-82-2/Bradykinin; 7440-09-7/Potassium; 7440-70-2/Calcium; 7665-99-8/Cyclic GMP; 80408-46-4/STA 2; EC Oxide Synthase

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