Atrial natriuretic peptide in alcoholic cirrhosis

Sodium retention in cirrhosis could result from a deficiency of atrial natriuretic peptide (ANP) or end‐organ resistance to ANP. Venous levels of α‐human ANP (αhANP) measured in 19 alcoholic cirrhotics by radio‐immunoassay were in the higher end of the normal range (29.7 pg/ml, s.d. = 17.2) and tended to increase with development of ascites or varices. Arterial levels of αhANP were not related to right atrial pressure but were related inversely to pulse rate. There was significant splanchnic (mean = 37.2%, s.d. = 19.5) and non‐splanchnic clearance (mean = 30.3%, s.d. = 17.1) of αhANP. The percentage extraction of αhANP across the splanchnic bed (%E ANP splanchnic) was not related to portal pressure, effective hepatic plasma flow or degree of intrahepatic shunting. The %E ANP splanchnic increased as functional liver cell mass (antipyrine clearance) decreased (r= 0.592, P= 0.034). Despite increased splanchnic clearance, αhANP levels increased with a fall in functional liver cell mass presumably due to increased release. Renal sodium retention in cirrhosis does not involve a deficiency of αhANP but increased end‐organ resistance needs to be excluded.