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Current Topics in Peptide & Protein Research   Volumes    Volume 4 
Atrial natriuretic peptides: modulation of other peptide and / or steroid hormones
David L. Vesely
Pages: 97 - 112
Number of pages: 16
Current Topics in Peptide & Protein Research
Volume 4 

Copyright © 2001 Research Trends. All rights reserved


Atrial natriuretic peptides are a family of peptides which are synthesized and stored as three different prohormones (i.e., 126 amino acid [a.a.] atrial natriuretic peptide (ANP), 108 a.a. brain natriuretic peptide and 126 a.a. C-natriuretic peptide prohormones). The peptide hormones derived from these prohormones have diuretic, natriuretic and blood pressure lowering properties. Recent evidence suggests that the peptide hormones derived from the ANP prohormone have significant interrelationships with other hormonal systems. Thus, atrial natriuretic peptides consisting of a.a. 1-30 (i.e., long acting natriuretic hormone), a.a. 31-67 (vessel dilator), a.a. 79-98 (kaliuretic hormone) and a.a. 99-126 (ANP) of the 126 a.a. ANP prohormone each decrease the circulating  concentrations of corticotropin releasing hormone (62%-84% decrease), corticotropin (i.e., ACTH, 58-81% decrease) and cortisol (67%-73% decrease) in healthy humans when these respective peptides are infused at their 100 ng/kg·bodyweight·min concentrations for 60 minutes. These peptide hormones also decrease the circulating concentration of prolactin from the pituitary while increasing leutinizing hormone (LH) release from the pituitary. The increase of LH in the circulation results in an increase in testosterone in the circulation secondary to these peptide hormones. These four cardiac peptides also decrease the circulating concentration of thyroxine (T4) and triiodothyronine (T3) with a resultant increase in thyroxine-stimulating hormone (TSH) suggesting that they inhibit thyroglobulin proteolysis.

These peptide hormones appear to be part of a negative feedback regulating-pathway with T3, T4, and cortisol, each of which enhance the gene expression of these four peptide hormones with a resultant increase in each of these four peptide hormones within the circulation. These peptide hormones also decrease aldosterone and/or plasma renin activity as well as modulate the circulating concentrations of calcitonin-gene related peptide, adrenomedullin and endothelin. There, thus, appears to be a intricate interrelationship of these four cardiac hormones with other peptide and / or steroid hormones.

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