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Horm Metab Res 1989; 21(9): 519-522
DOI: 10.1055/s-2007-1009275
Clinical

© Georg Thieme Verlag, Stuttgart · New York

Atrial Natriuretic Factor in Liver Cirrhosis - The Influence of Volume Expansion

V. Tesař1 , K. Horký2 , J. Petrýl1 , M. Kozáková1 , I. Gregorová2 , M. Brodanová1 , V. Kordač1 , M. Hirsa1  Jr. 
  • 11st Department of Medicine, Faculty of Medicine, Charles University, Prague, Czechoslovakia
  • 23rd Department of Medicine, Faculty of Medicine, Charles University, Prague, Czechoslovakia
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Publikationsverlauf

1988

1989

Publikationsdatum:
14. März 2008 (online)

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Summary

Plasma levels of atrial natriuretic factor (ANP) were examined in 12 patients with liver cirrhosis (6 with ascites) and 6 controls before and after the administration of the infusion of 2000 ml of saline solution per 70 kg of body weight during 2 hours. Basal concentration of ANF tended to be slightly, but nonsignificantly higher in patients with ascitic liver cirrhosis (5.5 ± 1.3 fmol/ml) than in controls (3.0 ± 1.0 fmol/ml) and in patients with non-ascitic liver cirrhosis (4.6 ± 1.3 fmol/ml). Saline administration led to the comparable increase of plasma ANF in ascitic (14.2 ± 4.0 fmol/ml) and non-ascitic cirrhotics (15.7 ± 3.7 fmol/ml) and in controls (12.4 ± 4.3 fmol/ml). The increase of plasma ANF was accompanied by the suppression of plasma renin activity (PRA) and plasma aldosterone (PA) in all groups; in ascitic patients, however, PRA and PA remained above the normal range. While in controls and non-ascitic cirrhotics saline administration led to the increase of urine flow rate /from 0.74 ± 0.13 to 2.04 ± 0.44 ml/min, P < 0.01, in controls; from 0.83 ± 0.05 to 1.28 ± 0.07 ml/min, P < 0.01, in non-ascitic cirrhotics) and urinary sodium excretion (from 110.7 ± 21.3 to 364.8 ± 74.4 umol/min, P < 0.01, in controls; from 125.0 ± 16.7 to 218.7 ± 24.3 umol/min, P < 0.01 in non-ascitic cirrhotics), in patients with ascetic liver cirrhosis neither urine flow rate (from 0.66 ± 0.1 to 0.72 ± 0.15 ml/min, n. s.), nor urinary sodium excretion (from 16.7 ± 9.9 to 54.2 ± 40.3 umol/min, n. s.) changed significantly.

Our results suggest that the increase of ANF is not the only mechanism responsible for sodium excretion after saline infusion. Its renal effect can be modified by other humoral and non-humoral factors. In ascitic liver cirrhosis the incomplete suppression of PRA and PA during saline infusion could participate in the “resistance” to the renal action of ANF increased to the same levels as in controls.

Key-Words

Atrial Natriuretic Factor - Plasma Renin Activity - Aldosterone - Liver Cirrhosis - Ascites

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