No description available.

Taurine transport in purified brush-border membranes from rodent kidney is concentrative and driven by the Na('+) gradient and transmembrane potential difference. The high-affinity, low-capacity carrier is specific for (beta)-amino compounds. / Inherited, strain-dependent influences on taurine reabsorption were investigated in the C3H/HeJ strain, a low excretor of taurine in urine and the C57Bl/6J strain, a high excretor. Although both strains transport taurine similarly at the luminal membrane, impaired exit at the baso-lateral membrane of renal epithelium in the hypertaurinuric strain results in increased intracellular levels of taurine and subsequent backflux into the urine. / The kidney is an important arbiter of taurine homeostasis. When animals are deprived of taurine, the kidney adapts by increasing taurine uptake at the renal brush-border membrane and in renal cortex slices; fractional excretion drops sharply. A change in plasma taurine may be the critical signal for adaptation.

Thesis (M.D.)--University of Adelaide, 1987. / Includes bibliographical references (leaves x-xxii).

Thèses (Ph.D.)--Université de Sherbrooke (Canada), 1997. / Titre de l'écran-titre (visionné le 20 juin 2006). Publié aussi en version papier.

Taurine (2-aminoethane sulfonic acid) is one of the most abundant free amino acids found in mammalian brain, heart and muscle. Taurine levels have also been shown to be altered in certain disease states. A physiological role for taurine in the maintainance of excitatory activity in muscle and nervous tissues has been suggested; however its possible mechanism of action is still uncertain. Early work on the pharmacological actions of taurine involved its possible conversion to isethionic acid (2-hydroxyethane sulfonic acid), a strong anion. This conversion was said to lead to the conductance of cations into the cardiac cell. An analytical technique to measure isethionic acid in mammalian tissues was developed. The method involved extraction, partial purification and methylation with diazomethane, followed by gas-liquid chromatography. With this technique only trace amounts of isethionic acid were detected in rat heart (0.1 mg/lOOg wet weight tissue) and rat brain (0.2 mg per 100 mg wet weight tissue) and none was detected in dog hearts. Recovery of added isethionic acid was between 95 and 100%. The assay was validated using a sample of squid axoplasm. We were also unable to show ¹⁴C-taurine conversion to ¹⁴C-isethionic acid in rat heart slices. Theories on the mode of action of taurine involving bioconversion to isethionic acid were therefore questioned. Some recent work suggested that taurine affects calcium kinetics in perfused guinea-pig hearts and calcium transport in rat skeletal muscle sarcoplasmic reticulum. We have investigated the effect of taurine on ATP-dependent calcium binding and oxalate-dependent calcium uptake in crude preparations of guinea-pig sarcolemma and in microsomal preparations enriched in sarcoplasmic reticulum. Taurine (5-50 mM) was found to have no significant effect on either ATP-dependent Ca²⁺ binding or uptake in both preparations. This result was observed at all calcium concentrations tested (0.5-100 uM) and at all incubation times used (30 seconds to 20 minutes). Taurine (20 mM) neither altered the effect of cyclic AMP-dependent protein kinase on oxalate-dependent calcium uptake nor exerted a stabilization action on calcium transport in these systems. In a further attempt to determine the possible physiological role of taurine in mammalian tissues, we have investigated the effect of taurine on passive transport of sodium, potassium and calcium in synaptosomal preparations of rat brain. Taurine, in a dose dependent manner, was found to have an inhibitory effect on both calcium- uptake and release in these preparations. Amino acids structurally similar to taurine ( β- alanine, homotaurine, hypotaurine and ɣ- aminobutyric acid) were also shown to inhibit calcium uptake in these preparations while a - alanine, proline and valine had no significant effect. Taurine (20 mM), though, did not alter the permeability of these preparations to either sodium or potassium. It thus appeared that taurine, and chemically related amino acids, can specifically alter calcium movements in these preparations. It is suggested that this effect is due to the binding of these agents to taurine receptor sites postulated to be present in these membranes. These observations may help to provide an insight into the physiological and pharmacological effects of taurine reported in cardiac and nervous tissues. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

No description available.

Taurine (2-aminoethane sulfonic acid) is one of the most abundant inhibitory amino acids in the mammalian central nervous system (CNS). Substantial evidence exists to suggest that this amino acid is a physiological modulator of neuronal excitability. Taurine is also a potent anticonvulsant in a variety of animal epilepsies and in certain human epileptics. The mechanisms of these neuromodulatory and anticonvulsant actions of taurine are not known. I have investigated a proposed relationship between altered amino acid metabolism, seizure-susceptibility and the anticonvulsant action of taurine. The findings of the work presented in this dissertation indicate that in the genetically seizure-susceptible rat there are alterations in the subcellular concentration and transport of taurine. Furthermore, the data presented here indicate that these alterations in the CNS handling of taurine are not a consequence of seizure activity but rather may be contributing to the seizure-susceptibility. This supports the hypothesis that taurine is a physiological modulator of neuronal excitability and that defects in this neuromodulatory process may contribute to seizure-susceptibility. The action of taurine was found to not be mediated by a redistribution of glutamate in the brain but instead may be by increasing the conversion of glutamate to GABA.

No description available.

Bibliography: leaves x-xxii / xvii, 285, xxii leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, 1987

No description available.