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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2003; 49(5): 58-62


Effects of chronic acidosis onprotein metabolism

M. V. Kryshtal

    A.A. Bogomoletz National Medical University, Kiev


Abstract

In experiments on mongrel albino male rats, we studied the effects of 30 mmol/kg lactic acid, 30 mmol/kg NaHCO3</subsub>, and 20 mmol/kg NH4Cl (intraventricular injections, daily for 7 days) on the contents of total protein, residual nitrogen, urea, and creatinine in the blood, as well as on the activities of aldolase and alanine aminotranspherase (ALT). We also studied the effects of the above agents on renal functions: glomerular filtration rate (GFR), diuresis, and excretion of ammonium, creatinine, and protein with urine. We have found that chronic, hyperchloremic, and lactic acidosis resulted both in a significant decrease in the levels of protein and residual nitrogen and in an increase in the concentration of the urea; these phenomena were accompanied by a considerable intensification of the urinary NH4+ excretion. In contrast, under conditions of chronic alkalosis we observed a drop in the level of urea in the blood with no changes in the concentrations of protein and residual nitrogen, as well as a dramatic depression of the urinary NH4+ excretion. In that case, the concentration of creatinine in the blood, GFR, diuresis, and excretion of creatinine and protein with urine did not correlate with the above-mentioned changes in protein metabolism. In all experiments, the activities of aldolase and ALT preserved their normal level giving evidence against damage to the liver. These results give evidence for spending a great number of amino acids on the renal ammoniogenesis at chronical acidosis; their saving at alkalosis; an impairment of the protein synthesis, and an increase in protein catabolism at acidosis to replenish the pool of amino acids, as well as for an activation of the urea synthesis to eliminate the excessive amount of NH4+ from the blood.

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