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 Lee, F.-L.
Right arrow Articles by Trendelenburg, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, F.-L.
Right arrow Articles by Trendelenburg, U.
Journal of Pharmacology And Experimental Therapeutics, Vol. 155, Issue 2, 211-222, 1967
Copyright © 1967 by American Society for Pharmacology and Experimental Therapeutics

THE UPTAKE OF TYRAMINE AND FORMATION OF OCTOPAMINE IN NORMAL AND TACHYPHYLACTIC RAT ATRIA

F.-L. Lee 1, N. Weiner 1, and U. Trendelenburg 1

1 Department of Pharmacology, Harvard Medical School, Boston, Massachusetts

Isolated rat atria are able to take up rapidly H3-tyramine and convert it to octopamine, which is efficiently retained in the tissue. Tyramine (unlabeled) accelerates the release of the retained H3-amines. After a single exposure to 3 µg/ml of tyramine for 2 min, approximately 15% of the retained H3-amines is released. After 12 such exposures, 85% of the H3- amines is depleted. After a similar number of exposures to tyramine, rat atria develop tachyphylaxis to the positive chronotropic effect of both tyramine and octopamine, although the norepinephrine content of these atria is not significantly different from that of control atria. Tachyphylactic atria are similar to control atria with regard to their ability to convert tyramine to octopamine, but these atria, after a brief exposure to H3-tyramine, retain significantly greater amounts of the unchanged H3-amine. Norepinephrine partially restores the responsiveness of tachyphylactic rat atria to tyramine and partially reverses the increased retention of H3-tyramine by these atria. These data suggest that tyramine is able to release only a small portion of the norepinephrine from atria and when this pool is depleted the action of tyramine is impaired (tachyphylaxis). Tyramine is able to exchange efficiently with the tyramine (or octopamine) present in this pool, but the released tyramine (or octopamine) is without effect. Exposure to norepinephrine leads to partial replacement of the tyramine by norepinephrine and a partial restoration of the sensitivity to subsequent additions of indirectly-acting amine.

Submitted on April 27, 1966
Accepted on August 9, 1966




This article has been cited by other articles:


Home page
 ScienceHome page
W. Emlen, D. S. Segal, and A. J. Mandell
Thyroid State: Effects on Pre-and Postsynaptic Central Noradrenergic Mechanisms
Science, January 7, 1972; 175(4017): 79 - 82.
[Abstract] [PDF]

Home page
 ScienceHome page
D. S. Segal, J. L. Sullivan III, R. T. Kuczenski, and A. J. Mandell
Effects of Long-Term Reserpine Treatment on Brain Tyrosine Hydroxylase and Behavioral Activity
Science, August 27, 1971; 173(3999): 847 - 849.
[Abstract] [PDF]


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

Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics.