Isolated rat atria are able to take up rapidly H 3 -tyramine and convert it to octopamine, which is efficiently retained in the tissue. Tyramine (unlabeled) accelerates the release of the retained H 3 -amines. After a single exposure to 3 µg/ml of tyramine for 2 min, approximately 15% of the retained H 3 -amines is released. After 12 such exposures, 85% of the H 3 - 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 H 3 -tyramine, retain significantly greater amounts of the unchanged H 3 -amine. Norepinephrine partially restores the responsiveness of tachyphylactic rat atria to tyramine and partially reverses the increased retention of H 3 -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.
The uptake of tyramine and formation of octopamine in normal and tachyphylactic rat atria.
F. Lee,N. Weiner,U. Trendelenburg
Published 1967 in Journal of Pharmacology and Experimental Therapeutics
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- Publication year
1967
- Venue
Journal of Pharmacology and Experimental Therapeutics
- Publication date
1967-02-01
- Fields of study
Biology, Medicine, Chemistry
- Identifiers
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- Source metadata
Semantic Scholar, PubMed
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