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Abstract

It is well known that sodium retention occurs in a significant proportion of patients with cirrhosis despite normal supine plasma levels of renin, aldosterone (ALDO), and norepinephrine (NE). The current study was performed to assess whether this subset of patients also present normal activity of the renin-aldosterone and sympathetic nervous systems during upright posture in sitting position and moderate physical exercise. Nine healthy controls, 14 patients with compensated cirrhosis and 10 patients with cirrhosis, ascites, sodium retention, and normal supine plasma renin activity (PRA) and ALDO and NE concentration were sequentially studied after 60 minutes in supine rest, 30 minutes in sitting position, and 30 minutes of cycloergometric exercise (3-METs). Sitting position and exercise were associated with similar stimulation of the renin-aldosterone and sympathetic nervous systems in the three groups of subjects. Consequently, cirrhotic patients with ascites showed values of PRA and plasma concentration of ALDO and NE similar to healthy subjects and patients with compensated cirrhosis during supine rest (renin: 1.4 ± 0.3, 0.8 ± 0.2, and 0.8 ± 0.3 ng/mL.hr; aldosterone: 24.3 ± 4.7,20.2 ± 3.9 and 21.4 ± 3.4 ng/dL; norepinephrine: 252 ± 23, 250 ± 16, and 255 ± 23 pg/mL), sitting position (renin: 2.1 ± 0.5,1.1 ± 0.3, and 1.6 ± 0.4; aldosterone: 32.2 ± 7.3, 23.7 ± 5.3, and 26.2 ± 4.5; norepinephrine: 356 ± 38, 401 ± 63, and 420 ± 35), and exercise (renin: 2.9 ± 0.8, 1.6 ± 0.4, and 2.2 ± 0.5; aldosterone: 43 ± 6.4, 34.9 ± 8.5, and 38.2 ± 5.3; norepinephrine: 481 ± 35, 499 ± 54, and 534 ± 48). Plasma atrial natriuretic peptide concentration was significantly (P < .05) higher in cirrhotic patients with ascites than in healthy subjects during supine rest (5.69 ± 1.1 vs. 21.0 ± 3.3 fmol/L) and exercise (9.1 ± 2.2 vs. 28.3 ± 6.6). These results indicate that sodium retention in cirrhosis may occur in the setting of a normal activity of the endogenous neurohormonal antinatriuretic systems and high plasma levels of ANP. (Hepatology 1995; 22:479–487.)