Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 256: C1168-C1175, 1989;
0363-6143/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Ibe, B. O.
Right arrow Articles by Campbell, W. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ibe, B. O.
Right arrow Articles by Campbell, W. B.

AJP - Cell Physiology, Vol 256, Issue 6 C1168-C1175, Copyright © 1989 by American Physiological Society

ARTICLES

Regulation of synthesis of prostacyclin and HETEs in human endothelial cells

B. O. Ibe, J. R. Falck, A. R. Johnson and W. B. Campbell
Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas 75235.

Human umbilical endothelial cells in culture synthesize prostacyclin (PGI2), 15-hydroxyeicosatetraenoic acid (15-HETE), and 12-hydroxyeicosatetraenoic acid (12-HETE). The synthesis of these eicosanoids was measured by specific radioimmunoassays after stimulation by arachidonic acid, A23187, bradykinin, melittin, or histamine. Under all conditions, the synthesis of PGI2 paralleled and exceeded the synthesis of 15-HETE and 12-HETE. Indomethacin inhibited arachidonic acid-stimulated PGI2 and 15-HETE synthesis but enhanced 12-HETE synthesis. Meclofenamate gave similar qualitative results. Drugs that act as inhibitors of lipoxygenase in some tissues, such as nordihydroguaiaretic acid (NDGA), caffeic acid, esculin, diethylcarbamazine, quercetin, and 5,8,11,14-eicosatetrayenoic acid (ETYA) were nonspecific in their inhibition of PGI2, 12-HETE, and 15-HETE synthesis. For example, NDGA inhibited arachidonic acid-stimulated release with a 50% inhibitory concentration (IC50) of 0.39 microM for PGI2, 0.25 microM for 15-HETE, and 0.10 microM for 12-HETE. These results show that endothelial cells metabolize both endogenous and exogenous arachidonic acid to PGI2, 15-HETE, and 12-HETE. These data also suggest, based on results with inhibitors, that PGI2 and 15-HETE are products of cyclooxygenase, whereas 12-HETE is produced via a different enzymatic pathway, most likely a lipoxygenase pathway.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Jayachandran, A. Sanzo, W. G. Owen, and V. M. Miller
Estrogenic regulation of tissue factor and tissue factor pathway inhibitor in platelets
Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1908 - H1916.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
P. F. Pratt, M. Rosolowsky, and W. B. Campbell
Mediators of Arachidonic Acid–Induced Relaxation of Bovine Coronary Artery
Hypertension, July 1, 1996; 28(1): 76 - 82.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online