Effects of Taurine on Signal Transduction Steps Induced during Hypertrophy of Rat Heart Myocytes

Abstract

Angiotensin II plays an important role in the development of cardiac hypertrophy. One factor thought to contribute to the trophic activity of angiotensin II in fibroblasts is the elevation in [Ca²⁺]_i. Although this theory has received considerable support in cardiac fibroblasts, it is much more controversial in cardiac myocytes. Therefore, the aim of this report was to examine the effect of several Ca²⁺ modulators on protein synthesis in neonatal cardiac myocytes. We found that angiotensin II increased both [Ca²⁺]_i and the rate of protein synthesis in isolated myocytes. Both effects were blocked by nifedipine, but only the angiotensin II-mediated increase in [Ca²⁺]_i was inhibited by taurine in a dose-dependent manner. These data support the notion that Ca²⁺ plays only a permissive role in angiotensin II-mediated stimulation of protein synthesis. By contrast, the ability of taurine to attenuate the positive chronotropic effect, the prolongation of the action potential and the proarrhythmic activity of angiotensin II appear to be linked directly to changes in [Ca²⁺]_i. We conclude that taurine reverses these actions of angiotensin II by altering Ca²⁺ flux across the cell membrane.