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Atrial Natriuretic Hormone, Vessel Dilator, Long-Acting Natriuretic Hormone, and Kaliuretic Hormone Decrease the Circulating Concentrations of Total and Free T₄ and Free T₃ with Reciprocal Increase in TSH

University of South Florida Cardiac Hormone Center; Departments of Biochemistry, Molecular Biology, Internal Medicine, Physiology, and Biophysics, University of South Florida Health Sciences Center; and James A. Haley Veterans Medical Center, Tampa, Florida 33612

Address all correspondence and requests for reprints to: David L. Vesely, M.D., Ph.D., Department of Endocrinology, Diabetes, and Metabolism, James A. Haley Veterans Hospital 151, 13000 Bruce B. Downs Boulevard, Tampa, Florida 33612. E-mail: vesely.david_l{at}tampa.va.gov

Abstract

The present investigation was designed to determine whether atrial natriuretic peptides (ANPs) consisting of amino acids 1–30 [i.e. long-acting natriuretic hormone (LANH)], 31–67 (vessel dilator), 79–98 (kaliuretic hormone), and 99–126 (atrial natriuretic hormone [ANH]) of the 126-amino acid ANH prohormone decrease the circulating concentrations of total and free T₄ and/or free T₃ in healthy humans (n = 30). Vessel dilator, kaliuretic hormone, LANH, and ANH decreased the circulating concentrations of total T₄ by 61%, 58%, 47%, and 55% and of free T₄ by 60%, 67%, 79%, and 79%, whereas free T₃ decreased 72%, 67%, 71%, and 67% (P < 0.05 for each), respectively, when infused at 100 ng/kg BW·min for 60 min. Vessel dilator, kaliuretic hormone, LANH, and ANH simultaneously increased circulating TSH concentrations 4- to 12.5-fold (P < 0.004). The decreases in T₄ and T₃ with reciprocal increases in TSH lasted 2–3 h after cessation of the respective ANP infusions. The reciprocal increase in TSH with the decreases in T₄ and T₃ suggests that their modulation of T₄ and T₃ concentrations occurs in the thyroid rather than in the pituitary or hypothalamus, because TSH would be decreased in the circulation if their inhibitory effects were in either the hypothalamus or pituitary.