Atrial natriuretic peptide: renal effects in cirrhosis of the liver

Atrial natriuretic peptide is one of a family of natriuretic peptides thought to play a role in the altered sodium balance of advanced liver disease and ascites. Its level is usually increased in the plasma of cirrhotic patients, probably due to relative plasma volume expansion. When exogenous ANP is administered intravenously to dogs or rats with experimental liver cirrhosis and ascites, an heterogeneous natriuretic response is obtained with about half of the population not responding. Similar observations are recorded for patients with clinical cirrhosis. In dogs, attenuation of the ANP-induced natriuresis may depend on a reduction in renal cortical bradykinin activity. In patients with cirrhosis, the ability to release ANP in response to central volume expansion is dissociated from the accompanying natriuresis. Attenuation of the renal tubular response to ANP in this setting may be correlated to the degree of intrahepatic sinusoidal hypertension and associated augmented reflex sympathetic nervous activity to the kidneys. Actual tubular resistance to ANP may be due to reduced Na+ delivery to the inner medullary collecting duct and/or increased degradation of cyclic guanosine monophosphate.