Acute acidosis and renal arteriovenous differences of glutamine in normal and adrenalectomized rats

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Abstract
A fluorometric assay for blood glutamine [Gln] was developed using purified rat renal phosphate-dependent glutaminase. This assay was used to characterize the changes in arterial and renal venous Gln levels that occur in response to an acute acidosis in both normal and adrenalectomized rats. Stomach feeding normal rats 2.0 mmol NH4Cl/100 g body wt caused a 2-fold increase in arterial Gln and a significant renal arteriovenous difference of Gln. Significant increases in arterial concentrations and in renal arteriovenous difference of Gln were also observed after feeding 0.2-1.0 mmol NH4Cl/100 g. In contrast, feeding high levels of NH4HCO3 produced only a 40% increase in arterial Gln concentration but no significant renal extraction. A slight increase in the arterial concentration alone is not sufficient to stimulate renal Gln extraction. Low NH4HCO3 levels had no effect on either the renal arterial or venous Gln concentration of Gln. Adrenalectomized rats exhibited a decreased blood Gln concentration and an impaired ability to increase arterial levels in response to acute acidosis. A significant but lower than normal renal arteriovenous difference of Gln was evident at all levels of NH4Cl fed. Accordingly, the acute increase in arterial Gln concentration, which may facilitate its renal extraction and metabolism, may be mediated by adrenal hormones.