Key result
Low-dose enalapril regresses cardiac hypertrophy without lowering blood pressure in rats, decreasing alpha-1-adrenergic receptors.
Why the study?
It was unclear whether alpha 1- or beta-adrenergic receptors are altered during regression of cardiac hypertrophy induced by antihypertensive agents.
Does treatment with enalapril, bunazosin, or propranolol alter adrenergic receptors during regression of cardiac hypertrophy in rats?
Does treatment with enalapril, bunazosin, or propranolol alter adrenergic receptors during regression of cardiac hypertrophy in rats?
Low-dose enalapril decreases alpha 1-adrenergic receptor numbers independently of blood pressure reduction during regression of cardiac hypertrophy, suggesting modulation of peripheral sympathetic activity.
Answers are grounded in this paper and cite their sources.
Suggests BP-independent hypertrophy regression via adrenergic modulation in rats; leaves open translation to human hypertension therapy.
OBJECTIVE: To determine whether alpha 1- or beta-adrenergic receptors are altered during regression of cardiac hypertrophy produced by antihypertensive agents. DESIGN AND METHODS: 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 alpha 1-adrenergic antagonist (bunazosin) or a beta-adrenergic antagonist (propranolol) for 6 weeks to induce regression. The numbers of alpha 1- and beta-adrenergic receptors, haemodynamics, tissue noradrenaline content and tissue ACE activity were measured. RESULTS: 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 alpha 1- or beta-adrenergic receptors was unchanged by propranolol treatment, but the number of alpha 1-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 alpha 1-adrenergic receptors. The dissociation constants for alpha 1- and beta-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. CONCLUSION: Of the three drugs tested, only the low dose of enalapril affected adrenergic receptors during regression of cardiac hypertrophy, causing a decrease in alpha 1-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.
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Matsui et al. (1994) studied Cardiac hypertrophy. Enalapril, bunazosin, or propranolol vs. Other experimental groups was evaluated on Numbers of alpha 1- and beta-adrenergic receptors. A low dose of enalapril (3 mg/kg) caused regression of cardiac hypertrophy without reducing blood pressure and decreased the number of alpha 1-adrenergic receptors in rats.
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