JPET Introducing ALZET?ew Model 2006 Pump

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 Stone, C. A.
Right arrow Articles by Totaro, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stone, C. A.
Right arrow Articles by Totaro, J. A.
Journal of Pharmacology And Experimental Therapeutics, Vol. 144, Issue 2, 196-204, 1964
Copyright © 1964 by American Society for Pharmacology and Experimental Therapeutics

ANTAGONISM OF CERTAIN EFFECTS OF CATECHOLAMINE-DEPLETING AGENTS BY ANTIDEPRESSANT AND RELATED DRUGS

Clement A. Stone 1, Curt C. Porter 1, John M. Stavorski 1, Carl T. Ludden 1, and James A. Totaro 1

1 Merck Institute for Therapeutic Research, West Point, Pennsylvania

The antidepressant drugs, protriptyline, imipramine, amitriptyline and their desmethyl derivatives, have been demonstrated to be capable of inhibiting catecholamine depletion in hearts of mice induced by agr-methyl-meta-tyrosine, metaraminol, guanethidine and 6-hydroxydopamine. These antidepressants also antagonized the action of guanethidine in reduring responses of the cat nictitating membrane and cardioacceleration in the dog elicited by sympathetic nerve stimulation. Related agents demonstrated to possess all or part of these antagonistic actions include cocaine, tripelennamine, pipradrol, methyiphenidate, chlorpromazine, promazine and desmethylpromazine.

The catecholamine-depleting effect of 6-hydroxydopamine was more readily blocked by these agents, as reflected by smaller doses required to demonstrate antagonism. agr-Methyl-meta-tyrosine was next most readily influenced while metaraminol and guanethidine were the most resistant. Reserpine-induced depletion of heart was not reduced even by relatively large doses. In terms of potency, protriptyline proved to be the most active antagonist of the several agents studied, both in terms of preventing catecholamine depletion and antagonizing the neuron blocking action of guanethidine.

The findings are discussed in relation to other classes of agents found to have similar antagonistic actions versus catecholamine-depleting agents.

Submitted on October 7, 1963
Accepted on January 3, 1964




This article has been cited by other articles:


Home page
 ScienceHome page
L. Stein and C. D. Wise
Possible Etiology of Schizophrenia: Progressive Damage to the Noradrenergic Reward System by 6-Hydroxydopamine
Science, March 12, 1971; 171(3975): 1032 - 1036.
[Abstract] [PDF]

Home page
 ScienceHome page
W. D. Reid, F. J. E. Stefano, S. Kurzepa, and B. B. Brodie
Tricyclic Antidepressants: Evidence for an Intraneuronal Site of Action
Science, April 25, 1969; 164(3878): 437 - 439.
[Abstract] [PDF]


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

Copyright © 1964 by the American Society for Pharmacology and Experimental Therapeutics.