Hemodynamic alterations were studied to determine their role in isoproterenol-induced cardiac arrhythmias in the desoxycorticosterone acetate--saline-treat rat. Since epinephrine, a catecholamine possessing an alpha-adrenergic receptor agonist component, was considerably less potent as an arrhythmogenic agent, an elevation in blood pressure was thought to be protective against arrhythmias. Both albuterol, a beta2-adrenergic agonist, alone and epinephrine administered following tolazoline, an alpha-adrenergic blocking agent, decreased blood pressure to that of isoproterenol but failed to elicit significant arrhythmias. Phenylephrine administered prior to isoproterenol resulted in significant arrhythmias despite the maintenance of mean blood pressure at normal levels. The study shows that blood pressure alterations are not important in the etiology of isoproterenol-induced arrhythmias in the corticoid-pretreated rat.