Implications of the natriuretic peptide system in the pathogenesis of heart failure: diagnostic and therapeutic importance.
The natriuretic peptide family consists of at least 3 structurally similar peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). Under normal conditions, ANP is synthesized by the atrium and released in response to atrial stretch. This peptide plays an important role in sodium and water homeostasis and is involved in cardiovascular function. In contrast, BNP is synthesized primarily by the ventricles, and its circulatory concentrations are significantly elevated in profound congestive heart failure (CHF). While both plasma levels of ANP and BNP have been found to be increased in patients with various heart diseases, the elevation in circulatory BNP correlates better than ANP with the severity of CHF. Therefore, plasma BNP has been suggested (and lately used) to aid in the accurate diagnosis of heart failure in patients admitted to the emergency room with symptoms of decompensated heart failure. Furthermore, circulatory BNP has been utilized as a prognostic marker in CHF as well as a hormone guide in the evaluation of the efficacy of the conventional treatment of this disease state. In light of the cardiovascular and renal effects of BNP, which most likely exceed those of ANP, the former has been used as a therapeutic agent for the treatment of patients with acute severe CHF. Intravenous infusion of BNP into patients with sustained ventricular dysfunction causes a balanced arterial and venous vasodilatation that has been shown to result in rapid reduction in ventricular filling pressure and reversal of heart failure symptoms, such as dyspnea and acute hemodynamic abnormalities. Thus, the goal of this article is to review the physiology and pathophysiology of natriuretic peptides and the potential use of their circulating levels for diagnosis and treatment of heart failure.
Abassi
Zaid
Z
Department of Vascular Surgery, Rambam Medical Center, P.O. Box 9602, 31096 Haifa, Israel. abassi@tx.technion.ac.il
Karram
Tony
T
Ellaham
Samer
S
Winaver
Joseph
J
Hoffman
Aaron
A
D000450:Aldosterone / Q000502:physiology; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology / Q000627:therapeutic use; D010450:Endopeptidases / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D020097:Natriuretic Peptide, Brain / Q000502:physiology / Q000627:therapeutic use; D020098:Natriuretic Peptide, C-Type / Q000502:physiology / Q000627:therapeutic use; D045265:Natriuretic Peptides / Q000502:physiology* / Q000627:therapeutic use; D011480:Protease Inhibitors / Q000627:therapeutic use; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
D045265:Natriuretic Peptides; D011480:Protease Inhibitors; D020097:Natriuretic Peptide, Brain; D020098:Natriuretic Peptide, C-Type; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D010450:Endopeptidases