Atrial natriuretic peptide in hepatic cirrhosis: relation to stage of disease, sympathoadrenal system and renin-aldosterone axis.
58 patients (mean age 51 years) with cirrhosis of the liver were studied. 16 patients were compensated, 18 decompensated with ascites, and 24 decompensated and treated with diuretics. Basal plasma levels of atrial natriuretic peptide were not different between any groups of cirrhotic patients and 17 control subjects (mean age 43 years). In contrast, the sympathoadrenal system (plasma noradrenaline, plasma adrenaline) and renin/aldosterone were significantly activated in decompensated cirrhotics. Circulating ANP was not related to plasma noradrenaline and adrenaline, plasma renin activity, plasma aldosterone, blood pressure, heart rate, or urinary sodium/potassium excretion in any cirrhotic group. Despite established sodium and volume retention in decompensated cirrhosis, the results indicate that diminished effective blood volume fails to release atrial natriuretic peptide in a larger amount due to insufficient atrial stretching. After insertion of a peritoneovenous shunt in one patient for treatment of refractory ascites, plasma atrial natriuretic peptide, urinary volume and sodium excretion increased, whereas elevated plasma levels of noradrenaline, renin activity and aldosterone decreased markedly.[1]References
- Atrial natriuretic peptide in hepatic cirrhosis: relation to stage of disease, sympathoadrenal system and renin-aldosterone axis. Burghardt, W., Wernze, H., Diehl, K.L. Klin. Wochenschr. (1986) [Pubmed]
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