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Molecular forms and biological activity of atrial natriuretic factor in patients with cirrhosis and ascites
Author(s) -
Jiménez Wladimiro,
Gutkowska Jolanta,
Ginés Pere,
Arroyo Vicente,
Rivera Francisca,
Rodés Joan
Publication year - 1991
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840140405
Subject(s) - medicine , cirrhosis , atrial natriuretic peptide , endocrinology , ascites , peptide hormone , natriuretic peptide , hormone , heart failure
Patients with cirrhosis and ascites show sodium retention and normal or increased plasma levels of atrial natriuretic factor, a peptide with powerful natriuretic activity. To investigate whether this paradoxical observation could be related to a dysregulation in the process of synthesis and maturation of atrial natriuretic factor leading to abnormal molecular forms lacking biological activity, the chromatographic patterns of atrial natriuretic factor contained in plasma extracts from 10 patients with cirrhosis and ascites and 6 healthy subjects were compared. Atrial natriuretic factor from cirrhotic patients was also tested in two different radioreceptor assays, which detect the biologically active form(s) of this peptide. Patients with cirrhosis and ascites had higher plasma levels of atrial natriuretic factor (81.3 ± 8.5 pg/ml, p < 0.001) than control subjects (29.8 ± 3.2 pg/ml). High‐performance liquid chromatography analysis of atrial natriuretic factor showed an identical chromatographic pattern in cirrhotic patients and control subjects. Three peaks related to the atrial natriuretic factor prohormone were observed in cirrhotic patients and control subjects, accounting for 64%, 23% and 11% of the total atrial natriuretic factor in cirrhotic patients and 63%, 18% and 8% of the total atrial natriuretic factor in control subjects. The main peak eluted at the same position of synthetic human atrial natriuretic factor (Ser 99‐Tyr 126), which represents the major active form of the circulating hormone. Cirrhotic atrial natriuretic factor displayed the same ability to inhibit the binding of 125 I‐atrial natriuretic factor to rat glomerular and bovine adrenal membrane receptors as synthetic human atrial natriuretic factor. In conclusion this study demonstrates that atrial natriuretic factor of patients with cirrhosis and ascites has an equipotent binding activity to its receptor as to that of synthetic human atrial natriuretic factor and possesses the same molecular weight and biologically active forms as atrial natriuretic factor of normal subjects. These data indicate that in cirrhosis there is no dysregulation in the atrial natriuretic factor maturation process. (H EPATOLOGY 1991;14:601–607.)