TY - JOUR
T1 - Cardiac secretion of adrenomedullin in human heart failure
AU - Jougasaki, Michihisa
AU - Rodeheffer, Richard J.
AU - Redfield, Margaret M.
AU - Yamamoto, Kazuhiro
AU - Wei, Chi Ming
AU - McKinley, Linda J.
AU - Burnett, John C.
PY - 1996/5/15
Y1 - 1996/5/15
N2 - Adrenomedullin (ADM) is a newly discovered endogenous vasorelaxing and natriuretic peptide. Recently, we have reported that plasma ADM is increased in severe congestive heart failure (CHF) in humans and that increased immunohistochemical staining is observed in the failing human ventricular myocardium. The present study was designed to test the hypothesis that the failing human ventricle secretes ADM and that circulating ADM progressively increases with the severity of clinical CHF. Plasma ADM was significantly increased in human CHF (39.8±3.6 pg/ml, P < 0.001 vs. normal) as compared with normal subjects (14.4±2.7 pg/ml). Plasma ADM was increased in mild CHF (NYHA class II, 30.1±3.4 pg/ml, P < 0.01 vs. normal), moderate CHF (NYHA class III, 31.5±3.0 pg/ml, P < 0.01 vs. normal), and severe CHF (NYHA class IV, 66.1±9.4 pg/ml, P < 0.001 vs. normal). In 13 patients with CHF in whom plasma samples were obtained from aorta (AO), coronary sinus (CS) and anterior interventricular vein (AIV), there was a significant step-up in plasma ADM between AO and AIV (50.6±9.3 pg/ml and 62.1±11.1 pg/ml, respectively, P < 0.01) and between AO and CS (50.6±9.3 pg/ml and 58.6±11.4 pg/ml, respectively, P < 0.05). The current study demonstrates that the failing human heart secretes ADM in human CHF suggesting contribution to the increase in plasma ADM, and indicates for the first time an additional endocrine system of cardiac origin which is activated in human CHF and may function in cardiorenal regulation.
AB - Adrenomedullin (ADM) is a newly discovered endogenous vasorelaxing and natriuretic peptide. Recently, we have reported that plasma ADM is increased in severe congestive heart failure (CHF) in humans and that increased immunohistochemical staining is observed in the failing human ventricular myocardium. The present study was designed to test the hypothesis that the failing human ventricle secretes ADM and that circulating ADM progressively increases with the severity of clinical CHF. Plasma ADM was significantly increased in human CHF (39.8±3.6 pg/ml, P < 0.001 vs. normal) as compared with normal subjects (14.4±2.7 pg/ml). Plasma ADM was increased in mild CHF (NYHA class II, 30.1±3.4 pg/ml, P < 0.01 vs. normal), moderate CHF (NYHA class III, 31.5±3.0 pg/ml, P < 0.01 vs. normal), and severe CHF (NYHA class IV, 66.1±9.4 pg/ml, P < 0.001 vs. normal). In 13 patients with CHF in whom plasma samples were obtained from aorta (AO), coronary sinus (CS) and anterior interventricular vein (AIV), there was a significant step-up in plasma ADM between AO and AIV (50.6±9.3 pg/ml and 62.1±11.1 pg/ml, respectively, P < 0.01) and between AO and CS (50.6±9.3 pg/ml and 58.6±11.4 pg/ml, respectively, P < 0.05). The current study demonstrates that the failing human heart secretes ADM in human CHF suggesting contribution to the increase in plasma ADM, and indicates for the first time an additional endocrine system of cardiac origin which is activated in human CHF and may function in cardiorenal regulation.
KW - heart failure, congestive
KW - heart ventricle
KW - hormones
KW - myocardium
KW - peptides
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U2 - 10.1172/JCI118680
DO - 10.1172/JCI118680
M3 - Article
C2 - 8636418
AN - SCOPUS:0029976990
SN - 0021-9738
VL - 97
SP - 2370
EP - 2376
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 10
ER -