Adrenergic Reactivity in Hyperthyroidism

Timothy S. Harrison, MD; John H. Siegel, MD; William S. Wilson, MD; William J. Weber, MD
Arch Surg. 1967;94(3):396-402. doi:10.1001/archsurg.1967.01330090090023.
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THAT the clinical manifestations of hyperthyroidism depend upon the autonomic nervous system has been widely accepted since the experimental studies of Brewster et al1 in thyroid-fed dogs. Clinical studies in primary hyperthyroidism on the effects of reserpine,2 the effects of guanethidine,3 and on the response of the thyroid-treated subject to guanethidine4 have raised the question as to whether the effects of hypersecretion of thyroid hormone are due to a heightened sensitivity of effector organs to adrenergic stimuli or whether there is increased activity of the sympathetic nervous system as well. The recent studies of Horn-brook et al5 on the regulation of myocardial glycogen metabolism by thyroid hormone in rats suggest that thyroid administration produces a potentiation of catecholamine effects by causing an increased sensitivity of the myocardial catecholamine receptor site. This information plus that of DeGroot et al6 on the hyperkinetic circulation of resting


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