Studies on the mechanism of hydrocortisone potentiation of vasoconstrictor responses to epinephrine in the anesthetized animal

Abstract

The effect of hydrocortisone on vasoconstrictor responses to epinephrine, norepinephrine and sympathetic nerve stimulation was examined, using the perfused hindpaw of the dog and hindquarters of the cat. Hydrocortisone, 10 mg/kg, i.v., enhanced the response of epinephrine but not norepinephrine or nerve stimulation in both preparations and did not alter constrictor responses to several other sympathomimetic amines or dilator responses to isoproterenol or acetylcholine in hindquarter vessels. Augmentation of responses to epinephrine was absent when the dosage of hydrocortisone was increased to 100 mg/kg, i.v. or decreased to 1 mg/kg, i.v. Aldosterone, 0.1 mg/kg, i.v., also increased responses to epinephrine but not norepinephrine in the hindquarters whereas dexamethasone, 1 mg/kg, i.v., did not affect responses to either catecholamine. This effect of hydrocortisone did not appear to be attributable to a cocaine-like mechanism involving neuronal uptake of the amine nor to inhibition of catechol-O-methyl transferase (COMT). Although propranolol interfered with the ability of hydrocortisone to enhance responses to epinephrine, hydrocortisone lacked significant vascular β-adrenergic blocking activity, in that it did not modify dilator responses to isoproterenol. It is suggested that hydrocortisone augments vasoconstrictor responses to epinephrine by an action on adrenergic receptors.