Ontogeny of α 1-adrenergic receptors in the rat myocardium: Effects of hypothyroidism

Abstract

The effects of propylthiouracil (PTU) treatment on α 1- and β-adrenergic receptors in neonatal and adult rat myocardium were examined with the α 1-selective antagonist [ 3H]prazosin and β-antagonist (−)-[ 3H]dihydroalprenolol ((−)-[ 3H]DHA). Pre and postnatal PTU treatment (congenital hypothyroid state) decreased ventricular size and protein content at 15 and at 28 days (P < 0.01). Similarly PTU treatment after maturation (acquired hypothyroid state) is associated with decreased ventricular size and protein content (P < 0.01). PTU treatment did not alter ventricular DNA content at any age examined as compared to euthyroid controls. Specific [ 3H]prazosin binding to ventricular membrane increased with advancing postnatal age in both congenital hypothyroid pups and controls, reaching peak receptor density at 15 days of postnatal age (106 ± 8 vs. 151 ± 7 fmol·mg −1 protein). The density at 15 and 28 days was however significantly lower in hypothyroid pups (P < 0.01, P < 0.02). The effect of congenital hypothyroidism on (−)-[ 3H]DHA binding was more marked which significantly decreased from the first postnatal day. Acquired hypothyroidism is also associated with a decreased density of α 1- and β-adrenergic receptors in rat myocardium. We conclude that α 1- and β-adrenergic receptors are modulated by thyroid hormone in development well as mature stages of the rat.