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To determine whether α1- or β-adrenergic receptors are altered during regression of cardiac hypertrophy produced by antihypertensive agents.Cardiac hypertrophy was induced in rats by aortic banding. After 6 weeks banding the rats were treated with an angiotensin converting enzyme (ACE) inhibitor (enalapril), an α1-adrenergic antagonist (bunazosin) or a β-adrenergic antagonist (propranolol) for 6 weeks to induce regression. The numbers of α1- and β-adrenergic receptors, haemodynamics, tissue noradrenaline content and tissue ACE activity were measured.Regression of cardiac hypertrophy occurred after treatment of aortic banded rats with a high dose of enalapril, bunazosin or propranolol, and was accompanied by a reduction in systolic blood pressure. The number of α1- or β-adrenergic receptors was unchanged by propranolol treatment, but the number of α1-adrenergic receptors was increased in the hearts of rats treated with bunazosin. A low dose of enalapril (3 mg/kg body weight) caused regression of hypertrophy without a concomitant reduction in blood pressure, and decreased the number of α1-adrenergic receptors. The dissociation constants for α1- and β-adrenergic receptors were not different among the experimental groups, and the positive derivatives of left ventricular pressure was unaltered in rats treated with a low dose of enalapril but was reduced by the other drugs.Of the three drugs tested, only the low dose of enalapril affected adrenergic receptors during regression of cardiac hypertrophy, causing a decrease in α1-adrenergic receptor number without a reduction in blood pressure. This effect may be explained by non-haemodynamic actions of the ACE inhibitor enalapril, probably by modulation of peripheral sympathetic activity.