GLT1 and EAAC-1 are two important members of a family of sodium dependent transporters, which are largely responsible for glutamate and aspartate uptake in peripheral tissues (PalacÍn et al.1998). In the hypertrophic rat heart there is an increase in EAAC1 protein expression and a faster rate of aspartate transport compared to normal rat hearts (King et al. 2002) Nothing however is known about the expression of GLT1 in the hypertrophic heart or about the effect of cardiac hypertrophy on glutamate transport. The aim of this study was to investigate GLT1 expression and its contribution to glutamate transport in sarcolemmal vesicles prepared from control and hypertrophic heart. Hypertrophic hearts were obtained from spontaneously hypertensive rats, whilst normal hearts were obtained from their corresponding normotensive control, Wistar Kyoto rats. All rats were humanely killed by cervical dislocation and the hearts dissected. Cardiac sarcolemmal vesicles were prepared by homogenisation and differential centrifugation (King et al. 2001). The initial rate (at 1s) of 0-0.3mM L-[¹⁴C]glutamate transport was measured by rapid filtration at room temperature (King et al. 2001). These measurements were carried out with/without 0.2mM of the selective GLT1/EAAC-1 inhibitor, L-serine-O-sulphate (SOS) (Palacin et al.1998). Western blotting followed by scanning densitometry was used to assess the level of GLT1 expression (King et al. 2001).GLT1 was expressed in sarcolemmal vesicles from both normal and hypertrophic hearts. The density of the bands for vesicles from hypertrophic hearts was 11.42±1 1.1 optical density units (OD)/mm² which was significantly greater than the 7.28±0.62 OD/mm² measured for vesicles from normal hearts (N = 4±S.E., p>0.02, Students unpaired ttest). The maximal velocity of the SOS insensitive sodium dependent component of glutamate uptake was significantly faster at 5.7±1.2 pmol/mg/s in vesicles prepared from hypertrophic hearts compared to the 1.0±0.2 pmol/mg/s (N = 4±S.E., p < 0.01, Students unpaired ttest) measured for vesicles from control hearts. These results suggest that in comparison to the normal heart, the expression and activity of GLT1 is upregulated in the hypertrophic heart.