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Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans

¹Medizinische Unversitaetsklinik, Kantonsspital Bruderholz, CH-4101 Bruderholz/Switzerland; and ²Genentech, Incorporated, South San Francisco, California 94080

Submitted 13 August 2003 ; accepted in final form 10 September 2003

Ureagenesis in the liver consumes up to 1,000 mmol of /day in humans as a result of + urea + CO₂ + 3H₂O. Whether the liver contributes to the regulation of acid-base equilibrium by controlling the rate of ureagenesis and, therefore, consumption in response to changes in plasma acidity has not been adequately evaluated in humans. Rates of ureagenesis were measured in eight healthy volunteers during control, chronic metabolic acidosis (induced by oral administration of CaCl₂ 3.2 mmol·kg body wt^-1·day^-1 for 11 days), and recovery as well as during bicarbonate infusion (200 mmol over 240 min; acute metabolic alkalosis). Rates of ureagenesis were correlated negatively with plasma concentration both during adaption to metabolic acidosis and during the chronic, steady-state phase. Thus ureagenesis, an acidifying process, increased rather than decreased in metabolic acidosis. During bicarbonate infusion, rates of ureagenesis decreased significantly. Thus ureagenesis did not appear to be involved in the regulated elimination of excess . The finding of a negative correlation between ureagenesis and plasma concentration over a wide range of concentrations, altered both chronically and acutely, suggests that the ureagenic process per se is maladaptive for acid-base regulation and that ureagenesis has no discernible homeostatic effect on acid-base equilibrium.

acidosis; net acid excretion; alkalosis

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