Conference Article| October 01 1978 Recent Advances in the Study of the Disturbance of Electrolyte Transport in Bartter's Syndrome E. BOURKE; E. BOURKE 1Department of Medicine, Meath Hospital, Dublin, Ireland Search for other works by this author on: This Site PubMed Google Scholar V. DELANEY V. DELANEY 2Department of Medicine, Meath Hospital, Dublin, Ireland Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1978) 6 (5): 836. https://doi.org/10.1042/bst0060836a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation E. BOURKE, V. DELANEY; Recent Advances in the Study of the Disturbance of Electrolyte Transport in Bartter's Syndrome. Biochem Soc Trans 1 October 1978; 6 (5): 836. doi: https://doi.org/10.1042/bst0060836a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1978 Biochemical Society1978 Article PDF first page preview Close Modal You do not currently have access to this content.

Abstract. In man, HCl acidosis reduces blood and urinary urea with a concomitant rise in ammonium (NH+4) excretion. Significantly less urea is excreted following NH4Cl administration than following equimolar ingestion of NH4 HCO3. The results of these alterations in nitrogen excretion are interpreted in terms of bicarbonate utilization and production.

Mesangiocapillary glomerulonephritis due to mixed essential cryoglobulinaemia is reported in association with unilateral renal papillary necrosis. This previously unreported manifestation of cryoglobulinaemia supports the vascular theory of aetiology of papillary necrosis.

A simple method is described for the measurement of urinary oxalate. Oxalate decarboxylase is coupled with NAD+ requiring formate dehydrogenase and the result recorded spectrophotometrically. Accurate determination can be carried out either on urine or a citrate extract or urine. Using the citrate extract procedure, the urinary samples can be stored for at least 3 months without any effect on the oxalate content.

The interrelationships of [14C] glutamine metabolism and urea production were studied in the isolated perfused rat liver. Whereas urea formation remained linear throughout the perfusion period there was continuous utilisation and production of glutamine maintaining its concentration in the perfusate within the physiological range for rat plasma. Chronic NH4Cl induced metabolic acidosis did not effect either the production of urea or the turnover of glutamine, in marked contrast to findings in the whole animal.

Oedema results from excessive reabsorption of filtered sodium for the renal tubules. The reabsorption is not due to intrinsic alterations in tubular function but secondary to changes in the peritubular environment. Diuretics however act by blocking reabsorption in the tubules themselves. The mechanisms by which they produce their effects are still poorly understood. Advances in knowledge of the patterns of sodium transport at different parts of the nephron have enabled us to localize their sites of action in man. Application of this knowledge in patients with resistant oedema enables us to decide how to alter the type or dose of diuretic or diuretic combination.

A simple, rapid and specific method for the determination of [1-14C]lactose in biological fluids is described. It is based on the enzymic removal of the 1-14C atom of lactose as [14C]carbon dioxide, using commercially available enzymes. The assay involves only one critical addition and the entire reaction can be carried out in a scintillation vial.

1. The effects of oral hydrochloric acid, ammonium chloride, sodium bicarbonate and ammonium bicarbonate on urea and ammonium excretion in rats on a constant diet were studied. 2. Hydrochloric acid acidosis significantly reduced urea excretion in the rat, with an equimolar increase in NH+4 excretion and no change in their sum. In ammonium chloride acidosis, most of the additional nitrogen intake is excreted as NH+4 and a small percentage as urea. The converse holds true after administration of ammonium bicarbonate. The physiological significance of this is discussed. 3. The shift in nitrogen excretion from urea to NH+4 in acidosis is interpreted on the basis of bicarbonate production and utilization. Urea formation utilizes HCO-3. For amino acid sources, this utilization is offset by the metabolism of the carbon skeleton, which gives rise to HCO-3. When waste nitrogen is excreted as NH+4, no bicarbonate is utilized and the new HCO-3, generated by the carbon skeleton, hels to maintain hydrogen ion homeostasis.

Ireland has an effective National Drugs Advisory Board. Ethical considerations for human experimentation are unifonn throughout the country. The need for full‐time clinical pharmacology units has gained acceptance, but none has yet been established. Nonetheless, a contribution is being made to research in the field of clinical pharmacology.

Hydrochloric-acid induced acidosis reduced urea excretion in the rat, with an equimolar increase in NH+4 excreation and no change in their sum. By contrast, in the guinea pig, where ammonium excretion is small, HC1 administration did not effect urea excretion. Ammonium administered as NH4HCO3 was excreted mainly in the form of urinary urea, whereas that administered as NH4C1 was mainly in the form of ammonium. Methionine sulphoximine did not impair the increased ammonium excretion induced by acidosis, but did lead to a marked decrease in plasma glutamine levels and an overall increase in total urinary urea and ammonium nitrogen excretion. A reinterpretation of some aspects of the adaptations to metabolic acidosis is made based on these findings.

Using D-[1-(14)C]glucose as a tracer, renal glucose utilization and production was measured in chronic metabolic acidosis and alkalosis in dog kidney in vivo. In six experiments in acidosis, mean total renal glucose production was 4.447+/-1.655 SE mumol/min and glucose utilization was 4.187+/-0.576 SE mumol/min. In five alkalotic experiments it was found that mean total glucose production was 12.227+/-2.026 SE mumol/min and glucose utilization was 18.186+/-2.054 SE mumol/min. Renal glucose utilization and production are therefore significantly higher in alkalosis than in acidosis in vivo. Since glucose production is maximal under conditions when glutamine extraction is minimal (i.e. alkalosis), it is apparent that in alkalosis glutamine is not a major precursor of glucose.

A Case of nephrogenic diabetes insipidus due to extensive sarcoid infiltration of the kidney is reported. Serum and urinary calcium were normal. Significant renal functional improvement followed administration of steroids. Repeat renal biopsy after one year suggested significant histological improvement.

A new method is described that uses three commercially available enzymes for the estimation of the specific activity of glucose. It is based on the enzymic removal of the 1-14C of glucose as 14CO2 for the radioactive assay and on the spectrophotometric change at 340 mμ associated with the conversion to gluconate 6-phosphate for the nonradioactive assay. The method is specific, reproducible, and simple, involves only one critical addition, and gives over 98% recoveries in aqueous solutions and plasma.

Research Article| July 01 1972 Studies on glycolysis in the dog kidney in vivo J Costello; J Costello 1Department of Clinical Medicine and Biochemistry, Trinity College, Dublin 2, Irish Republic Search for other works by this author on: This Site PubMed Google Scholar J M Scott; J M Scott 1Department of Clinical Medicine and Biochemistry, Trinity College, Dublin 2, Irish Republic Search for other works by this author on: This Site PubMed Google Scholar P Wilson; P Wilson 1Department of Clinical Medicine and Biochemistry, Trinity College, Dublin 2, Irish Republic Search for other works by this author on: This Site PubMed Google Scholar E Bourke E Bourke 1Department of Clinical Medicine and Biochemistry, Trinity College, Dublin 2, Irish Republic Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1972) 128 (3): 80P–81P. https://doi.org/10.1042/bj1280080Pb Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation J Costello, J M Scott, P Wilson, E Bourke; Studies on glycolysis in the dog kidney in vivo. Biochem J 1 July 1972; 128 (3): 80P–81P. doi: https://doi.org/10.1042/bj1280080Pb Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1972 The Biochemical Society1972 Article PDF first page preview Close Modal You do not currently have access to this content.

THE principal mechanism whereby excess hydrogen ions are excreted in man is by renal production of ammonia and subsequent urinary excretion as ammonium. The major and direct source of this renal ammoniagenesis is glutamine1. Two distinct metabolic pathways of glutamine metabolism have been demonstrated in rat, guinea-pig and dog. The intramitochondrial glutaminase I isoenzymes which hydrolyse glutamine to ammonia and glutamic acid and its subsequent deamidation to ammonia and 2-oxo-glutarate constitute the major metabolic route in the rat2. The extramitochondrial glutamine-aminotransferase-ω-amidase pathway (glutaminase II), however, has been shown to be important in the dog3. In man, whereas the glutaminase I pathway has been demonstrated4 there is no direct evidence for the latter metabolic pathway. We investigated this metabolic pathway using the alkyl substituted glutamine, L-γ-glutamylmethylamide. In contrast to glutamine, this substituted compound on deamidation yields methylamine5.