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Nongenomic Cardiovascular Effects of Triiodothyronine in Euthyroid Male Volunteers

Institute of Clinical Pharmacology, University Hospital of Mannheim, Faculty for Clinical Medicine Mannheim, University of Heidelberg (B.M.W.S., N.M., A.C.G., H.-C.T., M.F., M.C., M.W.), 68135 Mannheim, Germany; and Medical Department 4/Nephrology, University of Erlangen-Nürnberg (B.M.W.S.), 90471 Nürnberg, Germany

Address all correspondence and requests for reprints to: Martin Wehling, M.D., Institute of Clinical Pharmacology, Faculty of Clinical Medicine, Ruprecht Karls University of Heidelberg, Theodor Kutzer Ufer 1-3, 68167 Mannheim, Germany. E-mail: . martin.wehling{at}kpha.ma.uni-heidelberg.de

Abstract

T₃ has been shown to exert cardiovascular effects. These effects have not yet been defined with regard to the mode of action (nongenomic vs. genomic) and with regard to an interaction with the adrenergic system in humans. To address these issues we conducted a randomized, double blind, 6-fold cross-over trial in 18 healthy male volunteers. After pretreatment with the ß-agonist dobutamine, the ß-blocking agent esmolol, or placebo (0.9% NaCl), 100 µg T₃ or placebo were injected. Primary target variables were systemic vascular resistance (SVR) and cardiac output (CO) within 45 min after injection of T₃ vs. placebo after placebo pretreatment. Sympatho-vagal balance was assessed by measurement of heart rate variability.

T₃ caused a lower SVR and a higher CO than placebo (P < 0.001) after pretreatment with placebo. An increased low frequency (LF)/high frequency (HF) ratio (power in LF/power in HF band) after T₃ compared with placebo (P = 0.004) suggests an increase in sympathetic tone. After pretreatment with dobutamine, the effects of T₃ on SVR and CO were abolished, and the effect on LF/HF ratio was reversed. After pretreatment with esmolol, the effects on SVR and LF/HF ratio were reversed. Our data show, for the first time, nongenomic cardiovascular effects of T₃ in humans.

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