Panos, Marios Zenon; (1990) Atrial natriuretic peptide in liver disease with sodium retention. Doctoral thesis (M.D), UCL (University College London).

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Abstract

Plasma concentration of atrial natriuretic peptide (ANP), measured by radioimmunoassay, was increased in patients with cirrhosis and ascites as compared to age matched healthy controls under basal conditions and throughout 24 hours of observation. Nocturnal natriuresis in patients, between midnight and 0800 hours, coincided with a marked reduction in the activity of the renin-aldosterone system. During this period there was significant correlation between urine sodium and plasma AJP concentration, suggesting that a). ANP may have a role in nocturnal natriuresis in cirrhosis and b). a reduction of renin-aldosterone in recumbency, may allow the natriuretic effect of ANP to become manifest. In the course of therapeutic paracentesis for tense ascites, plasma ANP tended to rise initially, in parallel with an increase in cardiac output and a drop in right atrial pressure, findings consistent with atrial decompression. Investigation by 2D-echo-cardiography, confirmed the presence of compression of the right atrium in patients with tense ascites. Plasma concentration of AHP in patients with paracetamol-induced fulminant hepatic failure was similar to that in healthy controls, but was increased in the presence of severe renal failure. Alterations in fluid balance, induced by haemodialysis and infusion of Human Albumin solution, resulted in appropriate changes of plasma AJTP. These findings indicate that a), there is no deficiency of AITP in fulminant hepatic failure and b). known mechanisms of ANP release are not impaired. In rats with carbon tetrachloride-induced cirrhosis, plasma ANP concentration was higher than in control animals. In cirrhotic rats with impaired sodium excretion in-vivo, there was diminished natriuretic response to infusion of synthetic AJP at physiological and pathophysiological concentrations, suggesting that in this animal model of cirrhosis, renal resistance to the natriuretic action of ANP may contribute to sodium retention.

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