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Article has an altmetric score of 6

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Research Article Free access | 10.1172/JCI109019

Characterization of a Carrier-Mediated Transport System for Taurine in the Fetal Mouse Heart In Vitro

David S. Grosso, William R. Roeske, and Rubin Bressler

The Department of Pharmacology, University of Arizona Health Sciences Center, Tucson, Arizona 85724

The Department of Internal Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724

College of Medicine, Tucson, Arizona 85724

Find articles by Grosso, D. in: PubMed | Google Scholar

The Department of Pharmacology, University of Arizona Health Sciences Center, Tucson, Arizona 85724

The Department of Internal Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724

College of Medicine, Tucson, Arizona 85724

Find articles by Roeske, W. in: PubMed | Google Scholar

The Department of Pharmacology, University of Arizona Health Sciences Center, Tucson, Arizona 85724

The Department of Internal Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724

College of Medicine, Tucson, Arizona 85724

Find articles by Bressler, R. in: PubMed | Google Scholar

Published April 1, 1978 - More info

Published in Volume 61, Issue 4 on April 1, 1978
J Clin Invest. 1978;61(4):944–952. https://doi.org/10.1172/JCI109019.
© 1978 The American Society for Clinical Investigation
Published April 1, 1978 - Version history
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Abstract

Cardiac taurine levels are elevated in hypertension and congestive heart failure. A possible mechanism for this increase in taurine is an alteration of its uptake. We sought to identify and characterize a carrier-mediated transport system for taurine in the mammalian myocardium utilizing the fetal mouse heart in organ culture. Hearts from fetuses of 16-19 days gestational age used in these studies had an endogenous taurine content of 14.1±0.5 nmol/mg tissue.

The uptake of [3H]taurine was linear for up to 8 h. Taurine was accumulated against a concentration gradient as demonstrated by a net increase in taurine concentration when hearts were incubated in 0.5 mM taurine. [3H]Taurine uptake was saturable, Km = 0.44 mM, temperature dependent, and required sodium. The close structural analogues, hypotaurine and β-alanine, reduced [3H]taurine uptake by 87% when present in 100-fold excess. The α-amino acids alanine, α-aminoisobutyric acid, glycine, leucine, and threonine did not inhibit uptake. Other taurine analogues tested were guanidinotaurine, guanidinopropionic acid, γ-aminobutyric acid, 2-aminoethane phosphonic acid, aminomethane sulfonic acid, 3-aminopropane sulfonic acid, N-acetyltaurine, and isethionic acid. We conclude that a carrier-mediated transport system for taurine exists in the fetal mouse heart based on the demonstration of (a) temperature dependence, (b) saturability, and (c) structural selectivity of the uptake process. Transport was demonstrated to be mediated by a β-amino acid uptake system. In addition, taurine uptake was observed to be sodium dependent, energy dependent, and capable of accumulating taurine against a concentration gradient.

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Referenced in 2 patents
6 readers on Mendeley
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