Dual effects of taurine on membrane ionic conductances of rat skeletal muscle fibers.

Abstract

Taurine (2-aminoethane sulfonic acid) levels are high in excitable tissues of mammals, including skeletal muscle. However, its physiological role at the molecular level remain unclear. Results from our laboratory indicate that taurine is a membrane stabilizer. Taurine, applied in vitro, reduces membrane excitability of rat skeletal muscle by specifically increasing membrane chloride conductance (GCl) (3). In mammalian skeletal muscle, the electrical stability of sarcolemma is controlled by a large GCl. An abnormally low GCl is responsible for the hyperexcitability characteristic of myotonic muscles (1,21). It has been proposed that many pharmacological actions of taurine are due to interaction with a low affinity binding site on membrane phospholipids (14). In rat skeletal muscle, this amino acid might modify GCl by a direct action on the low affinity site, as suggested by the findings that taurine restores GCl lowered by 20,25-diazacholesterol, which indirectly affects chloride channels by altering the lipid environment of the sarcolemma (5). In order to evaluate better the interaction between taurine and its low affinity binding site, the effects of a series of newly synthetized analogues of taurine (Figure 1) have been tested in vitro, on rat skeletal muscle and compared with those of taurine and other well known analogues such as 3-aminopropane sulfonic acid (homotaurine) (10) and guanidinoethane sulfonate (14).