Altered Cardiac Retention of Exogenous Noradrenaline produced by Stress in Young Rabbits


AN impressive body of evidence indicates that cardiovascular reactivity either to sympathetic nerve stimulation or to injected catecholamines is considerably decreased in adrenalectomized animals1. The administration of adrenocortical hormones to such animals either improves or restores to normal the ability of the cardiovascular system to respond either to sympathetic nerve activity or to the injection of adrenaline or noradrenaline1. These considerations suggest that one result of stress-induced adrenocortical secretion in normal animals might be an enhanced response of the cardiovascular system to the catecholamines. In support of this idea, it has been reported2 that hydrocortisone increased the response of rabbit aorta to noradrenaline in vitro. Such potentiation could be caused by a decreased tissue-binding (that is, functional inactivation) of administered noradrenaline produced by the steroid. This suggestion was investigated by examining the influence of administered hydrocortisone on the sub-cellular distribution of tritiated noradrenaline in the rabbit heart.

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    Besse, J. C., and Bass, A. D., Fed. Proc., 23, 457 (1964).

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    Gillis, C. N., J. Pharmacol., 146, 54 (1964).

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    Dohan, F. C., and Lukens, F. D. W., Endocrinology, 42, 244 (1948).

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    Potter, L. T., and Axelrod, J., J. Pharmacol., 142, 291 (1963).

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GILLIS, C. Altered Cardiac Retention of Exogenous Noradrenaline produced by Stress in Young Rabbits. Nature 207, 1302–1304 (1965).

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