J Physiol Society Meetings
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Physiology in Press

First published online on September 27, 2002.
Copyright © 2002 by The Physiological Society
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
545/1/269    most recent
2002.022384v1
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Suzuki, Y.
Right arrow Articles by Itoh, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Suzuki, Y.
Right arrow Articles by Itoh, T.

Received April 11, 2002
Accepted after revision September 2, 2002

Reduced function of endothelial prostacyclin in human omental resistance arteries in pre-eclampsia

Y. Suzuki1*, Tomonori Hattori2, Junko Kajikuri2, Tamao Yamamoto3, Kaoru Suzumori4, and Takeo Itoh2

1 Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Nagoya City University, Mizuho-ku, Nagoya 467-8601, Japan
2 Department of Cellular and Molecular Pharmacology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan
3 Departments of Obstetrics and Gynecology and Cellular and Molecular Pharmacology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan
4 Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan

* To whom correspondence should be addressed. E-mail: og.yo{at}med.nagoya-cu.ac.jp.

It remains unclear in pre-eclampsia whether or not a functional change occurs in the role played by prostacyclin in endothelium-dependent relaxation in resistance arteries. We examined this using human omental resistance arteries (obtained from pre-eclamptic or normotensive pregnant women) in the presence of NG-nitro-L-arginine (L-NNA, an inhibitor of nitric oxide synthase). In endothelium-intact strips from both groups, 9,11-epithio-11,12-methano-thromboxane A2 (STA2, a thromboxane A2 mimetic) produced a contraction. Diclofenac (an inhibitor of cyclooxygenase) enhanced the STA2 contraction only in the normotensive pregnant group (1.4 times control, P < 0.01). In the presence of STA2, bradykinin (0.1 µM) produced an endothelium-dependent relaxation in both groups, the relaxation being significantly smaller for the pre-eclamptic group (P < 0.002). Diclofenac significantly attenuated the bradykinin-induced relaxation only for the normotensive pregnant group (31 % inhibition, P < 0.001). The bradykinin-induced membrane hyperpolarization consisted of diclofenac-sensitive and -insensitive components. The former, but not the latter, was significantly smaller in pre-eclampsia (-4.3 vs. -2.6 mV, P < 0.05). The concentrations of 6-keto-PGF1{alpha} (a stable metabolite of prostacyclin) in these arteries were significantly lower in pre-eclampsia in both the absence and presence of bradykinin (about 0.2-0.4 times the normotensive pregnant value in each case, P < 0.01). By contrast, both the relaxation and the membrane hyperpolarization in response to beraprost (10 nM, a stable analogue of prostacyclin) were similar between the two groups. We conclude that, in pre-eclampsia, a reduced part is played by prostaglandins in the endothelium-dependent relaxation seen in resistance arteries and that this may be due to a reduced production of prostacyclin by the endothelium.




This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
L. Luksha, H. Nisell, N. Luksha, M. Kublickas, K. Hultenby, and K. Kublickiene
Endothelium-derived hyperpolarizing factor in preeclampsia: heterogeneous contribution, mechanisms, and morphological prerequisites
Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2008; 294(2): R510 - R519.
[Abstract] [Full Text] [PDF]


Home page
JAMAHome page
R. J. Kaaja and I. A. Greer
Manifestations of Chronic Disease During Pregnancy
JAMA, December 7, 2005; 294(21): 2751 - 2757.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
Y.-L. Dong, K. E. Green, S. Vegiragu, G. D. V. Hankins, E. Martin, M. Chauhan, C. Thota, and C. Yallampalli
Evidence for Decreased Calcitonin Gene-Related Peptide (CGRP) Receptors and Compromised Responsiveness to CGRP of Fetoplacental Vessels in Preeclamptic Pregnancies
J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 2336 - 2343.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
K. Takeuchi, H. Watanabe, Q.-K. Tran, M. Ozeki, D. Sumi, T. Hayashi, A. Iguchi, L. J Ignarro, K. Ohashi, and H. Hayashi
Nitric oxide: inhibitory effects on endothelial cell calcium signaling, prostaglandin I2 production and nitric oxide synthase expression
Cardiovasc Res, April 1, 2004; 62(1): 194 - 201.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2002 The Physiological Society.