Taurine Transport by Reconstituted Membrane Vesicles

American Journal of Physiology-heart and Circulatory Physiology, 1981

European Journal of Pharmacology, 1986

Positive inotropic effect of some taurine-related compounds on guinea-pig ventricular strips perfused with low calcium medium, European J. Pharmacol. 124 (1986) 129-133.

Amino Acids, 1999

In pro-and eucaryotic life, cellular and subcellular compartments are separated by membranes and the regulated and selective passage of specific molecules across these membranes is a basic and highly conserved principle.

Biochemical Pharmacology, 1982

Taurine increases the calcium levels in guinea-pig ventricular strips at external calcium concentrations of 0.45, 0.9 and 1.8 mM. At 2.7 mM calcium, however, a decrease is observed. Analogous changes occur in contractile force. It is also seen that the superfusion of ventricular strips with taurine-free medium produces a decrease in taurine content at the end of 120 min superfusion. Taurine levels can be restored by superfusion with 10 mM taurine; a linear relationship exists between external taurine and internal taurine levels.

1981

Taurine is found in high concentrations in the mammalian heart. The mammalian heart s t r i c t ly regulates the level of cardiac taurine. Increased cardiac taurine concentrations have been observed in human and experimental animal heart models. However, the function of cardiac taurine is an enigma. Taurine transport in the fe ta l mouse heart was studied and shown to be chronically regulated by the osmotic environment of the myocardium. A dd itiona lly , a l l taurine transport was found to have an obligatory requirement fo r sodium. At 1 hour transport of [^H]-taurine increased 56 percent in the presence of 80 mosmols additional NaCl. No stimulation occurred with equismolar additions of other osmotic agents: sucrose, L i C l , choline chloride or glucose. At 19 hours a l l of the osmotic agents tested resulted in s ig n if ica n t stimulation of [ H ] t a u r in e transport due to an apparent increse in the V without s ig n if ic an t change in K . Acute m ct X ill hypernatremic a...

Canadian Journal of Physiology and Pharmacology, 2019

Taurine is a nonessential amino acid that has received much attention. Two organs, the heart and the brain, are known to produce their own taurine, but in very limited quantities. It is for this reason that supplementation with this amino acid is necessary. Today, taurine is present in almost all energy drinks. A very vast literature reported beneficial effects of taurine in hepatic dysfunction, gastrointestinal injury, kidney diseases, diabetes, and cardiovascular diseases. Most of its effects were attributed to its modulation of Ca2+homeostasis as well as to its antioxidant properties. In this review, we will focus on the current status of taurine modulation of the cardiovascular system and discuss future avenues for its use as a supplement therapy in a specific cardiovascular disease, namely hypertrophy, and heart failure.

Journal of Clinical Investigation, 1978

A B S T R A C T 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.

Biochemical Pharmacology, 1981

Taurine uptake by guinea-pig hypertrophic heart sarcolemma vesicles was sodium-dependent and kinetic analysis suggested the presence of only one uptake system. The apparent K,,, and V,,,,, were the following; 2.5 x 10 ' M and 0.43 pmoles.mg ' protein min-' respectively. The uptake was specific and was inhibited by all analogues tested, except isethionic acid. The uptake was also inhibited by NaF.

Journal of Molecular and Cellular Cardiology, 1988

Abnormal beating patterns were induced in spontaneously contracting cultured embryonic mouse myocardial cells either by elevating or by lowering extracellular calcium. At low calcium (0.4 mM), the number of beating cells and beating rate decreased while the number of arrhythmic cells increased. By contrast, at high calcium (20 mM), the number of beating cells decreased while beating rate and the number of arrhythmic cells increased. Addition of taurine (20 mM) to the medium attenuated the response to varying calcium; the taurine effect appeared to be specific since neither taurine analog tested (beta-alanine nor glycine) provided much protection against these abnormalities. The protective effect of taurine also appeared to differ from that of verapamil, which was effective only in decreasing beating rate in the high calcium condition. Uptake of 14C-taurine by the cells was higher at both low and high extracellular calcium when compared to the normal calcium (2 mM) concentration. The results raise the possibility that the protective effect of taurine on beating abnormalities caused by low or high calcium is related to taurine uptake.

Biochimica et Biophysica Acta (BBA) - Biomembranes, 1979

The effect of taurine on calcium binding to isolated rat heart sarcolemmal membrane was examined. Taurine was observed to increase calcium binding to the low affinity sites in both high sodium-low potassium and low sodiumhigh potassium buffers. Taurine was also seen to antagonize the inhibition of calcium binding to the sarcolemma caused by both verapamil and lanthanum. Nevertheless, membrane structural changes due to taurine could not be detected using the spin label ESR probe 2N14. A possible regulatory role of taurine is discussed.

Molecular and Cellular Biochemistry, 1998

Recent studies in heart cells have shown taurine to induce a sustained increase of both intracellular Ca2+ and Na+. These results led us to believe that the increase in Na+ by taurine could be due to Na+ entry through the taurine-Na+ cotransporter which in turn favours transarcolemmal Ca2+ influx through Na+-Ca2+ exchange. Therefore, we investigated the effect of β-alanine, a blocker of the taurine-Na+ cotransporter and low concentrations of CBDMB (a pyrazine derivative, 5-(N-4chlorobenzyl)-2′,4′-dimethylbenzamil), a Na+-Ca2+ exchanger blocker on taurine-induced [Ca]i increase in embryonic chick heart cells. Using Fura-2 Ca2+ imaging and Fluo-3 Ca2+ confocal microscopy techniques, taurine (20 mM) as expected, induced a sustained increase in [Ca]i at both the cytosolic and the nuclear levels. Preexposure to 500 μM of the blocker of the taurine-Na+ cotransporter, β-alanine, prevented the amino acid-induced increase of total [Ca]i. On the other hand, application of β-alanine did not reverse the action of taurine on total [Ca]i. However, low concentrations of the Na+-Ca2+ exchanger blocker, CBDMB, reversed the taurine-induced sustained increase of cytosolic and nuclear free calcium (in presence or absence of β-alanine). Thus, the effect of taurine on [Ca]i in heart cells appears to be due to Na+ entry through the taurine-Na+ cotransporter which in turn favours transarcolemmal Ca2+ influx through the Na+-Ca2+ exchanger.

Proceedings of the Western Pharmacology Society, 2007

Taurine has a number of physiological functions, e.g., in cell volume regulation and inhibitory neuromodulation. Taurine and its derivatives have also been tested as potential pharmacological agents in many pathological states. We endeavor here to review the present status of this investigation. Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid present in virtually all cells throughout the animal kingdom. In particular, it is enriched in electrically excitable tissues such as brain, retina, heart and skeletal muscles. In the central nervous system, taurine has been implicated in two major phenomena; in cell volume regulation [1-3] and in inhibitory neuromodulation or neurotransmission [4-7]. Its function as a neurotransmitter implies the existence of specific taurine receptors and the neuromodulatory role, an interference with functions of other transmitter systems. There is scant evidence to corroborate the first assumption, but ample for the latter. In ...

Journal of Molecular and Cellular Cardiology, 1986

The effect of taurine on ~-and/~-mediated positive inotropic effects was investigated in guinea-pig ventricular strips. Loading with taurine dose-dependently antagonized the phenylephrine-induced positive inotropic effect while it was ineffective on ]~-mediated positive inotropic effect. The superfusion with a taurine-free medium determined a loss of intracellular taurine, while the loading with 20 mM taurine prevented this depletion. Preincubation of cardiac membranes with different concentrations of taurine (1 to 20 mM) decreased 3Hprazosin binding, and the saturation curve obtained after preincubation of cardiac membranes with 20 mM taurine showed that taurine had a more marked effect on the number of" binding sites. In both experimental models, ]~-alanine did not mimic any taurine effects, suggesting that taurine acdons might be specific.

Biochemical Pharmacology, 1985

In isolated guinea-pig heart submitted to hypoxia in the absence of substrate and subsequent reoxygenation 1-20 mM taurine decreases LDH release and ventricular arrhythmias, and the recovery of normal electrical and mechanical activity is increased. The taurine effect is dose-dependent, and is not mimicked by ~alanine. Moreover, taurine reduces the increase in calcium gain of reoxygenated heart.

European Journal of Pharmacology, 1984

F. FRANCONI, I. STENDARDI, R. MATUCCI, P. FAILLI, F. BENNARDINI, G. ANTONINI and A. GIOTTI, lnotropic effect of taurine in guinea-pig ventricular strips, European J. Pharrnacol. 102 (1984) 511-514.