Effect of taurine on calcium paradox and ischemic heart failure

Kramer, Jay H.; Chovan, James P.; Schaffer, Stephen W.

doi:10.1152/ajpheart.1981.240.2.h238

Cited by 71 publications

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“…Previous reports have shown that large amounts of taurine are lost from the ischemic myocardium (9,11). Similarly, taurine is lost in large quantities from cardiomyocytes during chemical hypoxia (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Beneficial effect of taurine depletion on osmotic sodium and calcium loading during chemical hypoxia

Schaffer

Solodushko

Kakhniashvili

2002

American Journal of Physiology-Cell Physiology

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Cellular sodium excess is cytotoxic because it increases both the intracellular osmotic load and intracellular calcium concentration ([Ca2+]i). Because sodium levels rise during hypoxia, it is thought to contribute to hypoxic injury. Thus the present study tested the hypothesis that taurine-linked reductions in [Na+]i reduce hypoxia-induced cell injury. Taurine depletion was achieved by exposing isolated neonatal cardiomyocytes to medium containing the taurine analog β-Alanine. As predicted, the β-Alanine-treated cell exhibited less hypoxia-induced necrosis and apoptosis than the control, as evidenced by less swelling, shrinkage, TdT-mediated dUTP nick end labeling staining, and accumulation of trypan blue. After 1 h of chemical hypoxia, [Na+]i was 3.5-fold greater in the control than the taurine-deficient cell. Although more taurine was lost from the control cell than from the β-Alanine-treated cell during hypoxia, the combined taurine and sodium osmotic load was lower in the β-Alanine-treated cell. Taurine deficiency also reduced the degree of hypoxia-induced calcium overload. Thus the observed resistance against hypoxia-induced necrosis and apoptosis is probably related to an improvement in sodium and calcium handling.

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Section: Discussionmentioning

confidence: 99%

“…A good correlation has been found between the ischemia-induced increase in cellular water and the rise in intracellular sodium ( (18). Opposing the unfavorable influence of the three hyperosmotic events is the release of organic osmolytes from the hypoxic myocyte (9,11,26). One of the primary organic osmolytes in the heart is the amino acid taurine (6).…”

mentioning

confidence: 99%

Beneficial effect of taurine depletion on osmotic sodium and calcium loading during chemical hypoxia

Schaffer

Solodushko

Kakhniashvili

2002

American Journal of Physiology-Cell Physiology

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“…Under disease conditions, thus, an application of taurine may be expected to protect against injuries and damages of cardiac cells (4,6,9). The present study shows that a) increasing pCa levels enhanced the I f , but did not stimulate the spontaneous activity; b) taurine application enhanced the I f at all the pCa levels; c) with an increase in pCa levels, an enhancement induced by 10 mM taurine increased further, whereas an enhancement induced by 20 mM decreased; d) taurine decreased I CaL , but stimulated I CaT ; e) taurine inhibited I Kr but not I Ks ; f) taurine inhibited I ST ; and g) dysrhythmias often occurred.…”

Section: Discussionmentioning

confidence: 99%

Elecropharmacology of Taurine on the Hyperpolarization-Activated Inward Current and the Sustained Inward Current in Spontaneously Beating Rat Sino-Atrial Nodal Cells

Satoh

2003

J Pharmacol Sci

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Abstract. Modulation by taurine of the pacemaking activity and the underlying ionic currents, especially a hyperpolarization-activated inward current (I f ) and a sustained inward current (I ST ), in rat sino-atrial (SA) nodal cells was investigated at different pCa levels using a patch-clamp technique. Increasing pCa levels from 10 to 6 stimulated the spontaneous activity and simultaneously increased the I f . Application of taurine depressed more strongly the spontaneous activity at higher pCa levels. At all pCa levels, however, taurine (20 mM) increased the I f by 60.1 ± 1.7% (n = 8, P<0.001) at pCa 10 and by 48.0 ± 1.4% (n = 8, P<0.01) at pCa 7. At pCa 7, taurine (10 and 20 mM) decreased the sustained inward current (I ST ) by 13.3 ± 1.1% (n = 5, P<0.05) and by 38.1 ± 2.4% (n = 5, P<0.01), respectively. Taurine (20 mM) inhibited the L-type Ca 2+ current (I CaL ) by 35.8 ± 2.5% (n = 8, P<0.01), whereas taurine enhanced the T-type Ca 2+ current (I CaT ) by 29.3 ± 2.9% (n = 8, P<0.05). Also, taurine at pCa 7 decreased the delayed rectifier K + current; taurine at 20 mM inhibited the rapidly activated K + current (I Kr ) by 55.6 ± 3.3% (n = 6, P<0.001), but not the slowly activated K + current (I Ks ). Taurine often elicited dysrhythmias, dependent on taurine's concentrations and pCa levels. These results indicate that taurine causes a negative chronotropic effect due to the inhibitions of the pacemaking ionic currents such as I CaL , I Kr and I ST , and suggest that the I f and I CaT currents make a minor contribution to pacemaking activity in rat SA nodal cells.

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“…Taurine also prevents myocardial necrotic lesions associated with calcium overload [45][46][47]. Accumulation of 45Ca by retinal subcellular fractions isolated from the chick retina was decreased when taurine was present in the incubation medium [48].…”

Section: Discussionmentioning

confidence: 99%

The mechanism of neuronal resistance and adaptation to hypoxia

Schurr

Rigor

1987

FEBS Letters

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In this work we provide a theoretical explanation for the observations that: (i) young animals are more resistant to hypoxia than adult ones and (ii) repeated exposure to a hypoxic insult increases the tolerance of young animals and isolated brain tissue to that insult. Considered here is the role of taurine, a putative Ca 2+ transport modulator, in attenuating Ca 2+ influx and overload in brain tissue upon hypoxia. It is proposed that the higher resistance of young animals to hypoxia stems from their higher brain content of taurine as compared with adults. The increased resistance to lack of oxygen upon re-exposure to hypoxia may occur as a result of protein and coenzyme A (CoA) breakdown which leads to the accumulation of products like cystine, cysteine, cysteamine and other sulfur-containing compounds. Upon reoxygenation, these compounds are oxidized to form taurine, which in turn attenuates neuronal Ca 2+ accumulation. The sulfurcontaining compounds are considered to be natural scavengers of oxygen-derived free radicals which are formed upon reoxygenation and have been implicated as a major component in the process leading to ischemic/hypoxic brain damage. Repeated hypoxic insults bring about the formation of higher levels of taurine and hence the observed adaptation to oxygen lack. The hypothesis presented here is supported by experimental observations in our laboratory and those of others.

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Effect of taurine on calcium paradox and ischemic heart failure

Cited by 71 publications

References 0 publications

Beneficial effect of taurine depletion on osmotic sodium and calcium loading during chemical hypoxia

Beneficial effect of taurine depletion on osmotic sodium and calcium loading during chemical hypoxia

Elecropharmacology of Taurine on the Hyperpolarization-Activated Inward Current and the Sustained Inward Current in Spontaneously Beating Rat Sino-Atrial Nodal Cells

The mechanism of neuronal resistance and adaptation to hypoxia

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