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Responses to triiodothyronine are similar in normal mice and mice lacking receptors for sympathetic-nervous-system hormones

Thyroid Digest July 2004The background of the study. Thyroid hormones and sympathetic-nervous-system hormones (catecholamines) have similar cardiovascular and metabolic actions. This study evaluated the cardiovascular and metabolic actions of thyroid hormone in animals lacking receptors for catecholamines.

How the study was done. The study animals were normal mice and mice lacking the genes for all forms of the -catecholamine receptor. The two types of mice had similar weights and serum thyroxine (T4) and triiodothyronine (T3) concentrations. Cardiovascular responsiveness to -receptor activation was determined by measurements of cardiac dynamics and heart weight after administration of the -receptor-activating drug isoproterenol. Thyroid hormone responsiveness was determined in the same way, and also by measurements of cardiac genes and oxygen consumption after injections of T3 or saline for 14 days.

The results of the study. The mice lacking -receptors had a lower rate of oxygen consumption and a slower heart rate than the normal mice. Blood pressure, cardiac contractility, and cardiac weight were similar in the two groups. Treatment with isoproterernol increased heart rate and heart weight in the normal mice, but not in the mice lacking -receptors. Administration of T3 increased oxygen consumption similarly in normal mice and mice lacking -receptors, but body weight did not change. Heart rate and cardiac contractility increased to the same extent in both groups of mice; cardiac weight increased more in response to T3 in the normal mice.

The conclusions of the study. Mice with no -receptors and normal mice have similar cardiovascular and metabolic responses to T3, indicating that these actions of T3 are not mediated by activation of the sympathetic nervous system.

The original article. Bachman ES, Hampton TG, Dhillon H, Amende I, Wang J, Morgan JP, Hollenberg AN. The metabolic and cardiovascular effects of hyperthyroidism are largely independent of -adrenergic stimulation. Endocrinology 2004;145:2767-74.


 

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