Glucocorticoids modulate myocardial beta-adrenergic receptors, but this does not explain their enhancement of catecholamine action, suggesting another mechanism.
Should not change glucocorticoid use in cardiac patients; leaves open non-receptor mechanisms of catecholamine potentiation.
One action of glucocorticoids is to enhance the tropic effect of catecholamines on heart muscle. To test the hypothesis that this action of glucocorticoids is mediated by modulation of beta-adrenergic receptors, we characterized and quantified myocardial beta-adrenergic receptors in adrenalectomized and glucocorticoid-replaced rats. Adrenalectomy was associated with an increase in myocardial beta-adrenergic receptors, as measured by [3H]dihydroalprenolol binding (P less than 0.001). This increase occurred by 6 h, with no difference over time to 7 days. The administration of cortisol (80 mg/kg.day) to adrenalectomized rats prevented the increase in beta-adrenergic receptors (P less than 0.01). The data indicate that glucocorticoids modulate myocardial beta-adrenergic receptors. However, these results do not support the hypothesis that glucocorticoid enhancement of catecholamine action is mediated by these changes, suggesting that glucocorticoids exert this action at a level other than the beta-adrenergic receptor site.
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Abrass et al. (1981) studied this question.
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