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Divisions of Cardiology (D.D.S.), Endocrinology and Metabolism (D.L.V., G.I.S.M., I.H.), Departments of 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., Director, Atrial Natriuretic Peptides Research Laboratories, James A. Haley Veterans Hospital, 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 consisting of amino acids 130 (i.e. long-acting natriuretic hormone), 3167 (vessel dilator), 7998 (kaliuretic hormone), and 99126 (atrial natriuretic hormone) of the 126 amino acid atrial natriuretic hormone prohormone decrease CRH, ACTH, and/or cortisol in healthy humans (n = 30). Vessel dilator, kaliuretic hormone, long-acting natriuretic hormone, and atrial natriuretic hormone decreased the circulating concentration of CRH 84%, 74%, 67%, and 62% (P < 0.001 for each), respectively, when infused at 100 ng/kg body weight·min for 60 min. Vessel dilator, kaliuretic hormone, long-acting natriuretic hormone, and atrial natriuretic hormone decreased circulating ACTH concentrations 58%, 80%, 81%, and 70% (P < 0.001) and the circulating concentration of cortisol 73%, 72%, 73%, and 67% (P < 0.001), respectively. The decreases in CRH, ACTH, and cortisol lasted 11/2 to 3 h after cessation of the respective atrial natriuretic peptide infusions. These data, along with the knowledge that cortisol upregulates atrial natriuretic peptides gene expression and CRH and ACTH stimulate atrial natriuretic peptides release, suggest that these four atrial natriuretic peptides may be part of an intricate feedback system to help regulate cortisol concentrations via their ability to decrease the circulating concentration of CRH which, in turn, results in a decrease in ACTH and cortisol.
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