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(Circulation. 1997;96:592-598.)
© 1997 American Heart Association, Inc.

Articles

Effects of Thyroid Hormone on Cardiac ß-Adrenergic Responsiveness in Conscious Baboons

Brian D. Hoit, MD; Saeb F. Khoury, MD; Yanfu Shao, MD; Marjorie Gabel; Stephen B. Liggett, MD; ; Richard A. Walsh, MD

From the Division of Cardiology, University of Cincinnati (Ohio) Medical Center.

Background Many of the cardiovascular manifestations of thyroid hormone excess resemble those produced by sympathoadrenal stimulation. The objective of this study was to determine the effects of thyroid hormone excess on myocardial ß-adrenergic expression and responsiveness to infused agonists in the primate heart.

Methods and Results The responses of left ventricular isovolumic contraction (dP/dt_max) and relaxation () during graded dobutamine infusion were studied both before and after 4 weeks of thyroid hormone administration in 8 chronically instrumented baboons. At matched (atrially paced) heart rates, thyroid hormone significantly increased resting dP/dt_max (3073±1034 versus 2318±829 mm Hg/s, P<.05) and decreased (24.0±5.5 versus 28.2±5.4 ms, P<.05). The change from baseline for dP/dt_max and in response to ß₁-adrenergic stimulation was significant at each dobutamine dose (2.5 to 10 µg·kg^-1·min^-1), but when expressed as a percent change, it was similar before versus after thyroid hormone. Similar changes were found when ß₂-adrenergic stimulation was produced by terbutaline infusion in three additional baboons. ß-Adrenergic receptor (ßAR) expression was higher in five thyroxine-treated than in five control baboons (37.4±1.2 versus 15.7±3.2 fmol/mg, P<.001), and this was due to a greater increase in the ß₂AR (5.9±1.5 to 20.6±1.2 fmol/mg, P<.001) than the ß₁AR (9.7±1.7 to 16.8±0.1 fmol/mg, P<.01) subtype.

Conclusions In the primate heart, thyroid hormone produces positive inotropic and lusitropic effects in the resting state and upregulates both ß₁AR and ß₂AR, with the ß₂AR increase predominating. At equivalent rates, however, thyroid hormone excess does not appear to enhance the sensitivity of left ventricular contractility and relaxation to either ß₁- or ß₂-adrenergic stimulation.

Key Words: thyroid • receptors, adrenergic, beta • contractility

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