Key result
Thyroxine administration increases myocardial beta-adrenoreceptor concentration ~1.8-fold versus controls.
Why the study?
The study aimed to determine whether myocardial beta-adrenoreceptor concentrations increase due to thyroid hormone action or secondary hemodynamic changes and ventricular hypertrophy.
Thyroxine upregulates canine myocardial beta-adrenoreceptors independent of hypertrophy; leaves open relevance to human hyperthyroidism or clinical practice.
Myocardial beta-adrenoreceptors, assessed in membrane preparations of left ventricle by 3H-dihydroalprenolol binding, were compared in dogs following thyroxine administration (n = 6), aorto-caval fistula (n = 12), and in normal dogs (n = 7). 2. Left ventricular hypertrophy occurred in response to both aorto-caval fistula and thyroxine treatment. Yield of myocardial membrane between the different groups was not significantly different. 3. Binding site concentration (pmol/mg membrane protein) in dogs with aorto-caval fistulae was similar to that in normal dogs and was not significantly influenced by the presence or absence of cardiac failure, degree of hypertrophy or duration of fistula. 4. Thyroxine-treated dogs had an increased concentration of binding sites (c. 1.8-fold) compared with both fistula and normal groups, while binding affinities were similar in all groups. 5. The data suggest that beta-adrenoreceptor concentrations in myocardium increase as a direct result of thyroid hormone action rather than as a result of secondary haemodynamic changes or ventricular hypertrophy.
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Ho et al. (1981) studied Left ventricular hypertrophy (n=25). Thyroxine administration vs. Aorto-caval fistula and normal dogs was evaluated on Myocardial beta-adrenoreceptor binding site concentration (c. 1.8-fold increase). Thyroxine administration increased myocardial beta-adrenoreceptor binding site concentration by approximately 1.8-fold compared with fistula and normal control groups.
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