JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 Eggerman, T. L.
Right arrow Articles by Robertson, R. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Eggerman, T. L.
Right arrow Articles by Robertson, R. P.

Separate receptors for prostacyclin and prostaglandin E2 on human gel- filtered platelets

TL Eggerman, NH Andersen and RP Robertson

Human gel-filtered platelets (GFP) and radiolabeled prostacyclin (PGI2), prostaglandin (PG) E2 and PGE1 were used to ascertain whether PGI2 and PGs of the E series share a common receptor or have their own specific receptors on platelets. Attention was given to ensuring the proper experimental conditions to compensate for the rapid half-life of PGI2 at physiologic pH. Specific [3H] PGI2 binding to GFP was maximal at 5 min and pH 7.45. Scatchard analysis indicated a single class of binding sites with an apparent KD of 4.52 X 10(-8) M and 1130 sites per platelet. Approximately 90% of specifically bound [3H]PGI2 could be dissociated by excess unlabeled PGI2 by 5 min. The IC50 for PGI2 was 66 nM. By 5 min, PGE1 and PGE2 were only 7.17 and 0.03%, respectively, as potent inhibitors of binding. Maximal specific binding of either [3H]PGE2 or [3H]PGE1 to GFP occurred by 60 min. During 60-min incubations with [3H]PGE2, the IC50 values for PGE2 and PGE1 were 3 and 6 nM, respectively. When [3H]PGE1 was used, the IC50 values for PGE1 and PGE2 were 30 and 10 nM, respectively. To examine PGI2 competition for [3H] PGE2 and [3H]PGE1 binding sites, 5-min incubation periods were used. PGI2 was only 0.38% as potent an inhibitor of [3H]PGE2 compared to PGE2 and only 30% as potent an inhibitor of [3H] PGE1 compared to PGE1. Scatchard analysis of the 60-min competition experiments using [3H]PGE2 and [3H]PGE1 and the homologous unlabeled ligand yielded curvilinear plots in both instances.(ABSTRACT TRUNCATED AT 250 WORDS)

Volume 236, Issue 3, pp. 568-573, 03/01/1986
Copyright © 1986 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 CirculationHome page
H. Ma, A. Hara, C. Y. Xiao, Y. Okada, O. Takahata, K. Nakaya, Y. Sugimoto, A. Ichikawa, S. Narumiya, and F. Ushikubi
Increased Bleeding Tendency and Decreased Susceptibility to Thromboembolism in Mice Lacking the Prostaglandin E Receptor Subtype EP3
Circulation, September 4, 2001; 104(10): 1176 - 1180.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1986 by the American Society for Pharmacology and Experimental Therapeutics.