Characterization of a carrier-mediated transport system for taurine in the fetal mouse heart in vitro

D. S. Grosso, William R Roeske, R. Bressler

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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/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.

Original languageEnglish (US)
Pages (from-to)944-952
Number of pages9
JournalJournal of Clinical Investigation
Volume61
Issue number4
StatePublished - 1978

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Fetal Heart
Taurine
Sulfonic Acids
In Vitro Techniques
Alanine
Isethionic Acid
Sodium
Aminoisobutyric Acids
Amino Acids
Temperature
Organ Culture Techniques
Threonine
Leucine
Glycine
Gestational Age

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Characterization of a carrier-mediated transport system for taurine in the fetal mouse heart in vitro. / Grosso, D. S.; Roeske, William R; Bressler, R.

In: Journal of Clinical Investigation, Vol. 61, No. 4, 1978, p. 944-952.

Research output: Contribution to journalArticle

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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/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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N2 - 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/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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