JPET

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 Besse, J. C.
Right arrow Articles by Bass, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Besse, J. C.
Right arrow Articles by Bass, A. D.
Journal of Pharmacology And Experimental Therapeutics, Vol. 154, Issue 2, 224-238, 1966
Copyright © 1966 by American Society for Pharmacology and Experimental Therapeutics

POTENTIATION BY HYDROCORTISONE OF RESPONSES TO CATECHOLAMINES IN VASCULAR SMOOTH MUSCLE

John C. Besse 1 and Allan D. Bass 1

1 Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee

Potentiation by hydrocortisone (HC) of responses to catecholamines has been studied in the dog and in the aortic strip preparation. The site of the potentiating action of HC is at the adrenergic receptor level. This conclusion is supported by the observations that potentiation was obtained for both the alpha and beta adrenergic effects of catecholamines in vivo and in vitro. The failure to demonstrate potentiation by HC of the aortic strip responses produced by agents other than catecholamines (with one exception, synephrine) indicates that there is considerable specificity in the action of HC. The observation that potentiation was obtained in reserpine-treated tissues both with and without cocaine indicates that the action of HC is not dependent upon the integrity of the endogenous catecholamine stores. Evidence was not found for a direct relationship between the potentiating action of HC and membrane depolarization or the availability of extracellular calcium for the muscle response produced by a stimulating agent. It is suggested that HC increases the affinity of the catecholamine or possibly its p-hydroxy analog for the adrenergic receptor by modifying the interaction of the p-hydroxyl group in the molecule with the receptor.

Submitted on February 10, 1966
Accepted on May 15, 1966




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. Xiao, X. Huang, S. Bae, C. A. Ducsay, and L. Zhang
Cortisol-mediated potentiation of uterine artery contractility: effect of pregnancy
Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H238 - H246.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. E Ullian
The role of corticosteroids in the regulation of vascular tone
Cardiovasc Res, January 1, 1999; 41(1): 55 - 64.
[Full Text] [PDF]

Home page
 NEJMHome page
S. W.J. Lamberts, H. A. Bruining, and F. H. de Jong
Corticosteroid Therapy in Severe Illness
N. Engl. J. Med., October 30, 1997; 337(18): 1285 - 1292.
[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 © 1966 by the American Society for Pharmacology and Experimental Therapeutics.