Abstract
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.
Footnotes
- Received February 10, 1966.
- Accepted May 15, 1966.
- © 1966 by The Williams & Wilkins Company
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