The amino acid, taurine, is an important nutrient found in very high concen
tration in excitable tissue. Cellular depletion of taurine has been linked
to developmental defects, retinal damage, immundeficiency, impaired cellula
r growth and the development of a cardiomyopathy. These findings have encou
raged the use of taurine in infant formula, nutritional supplements and ene
rgy promoting drinks. Nonetheless, the use of taurine as a drug to treat sp
ecific diseases has been limited. One disease that responds favorably to ta
urine therapy is congestive heart failure. In this review, we discuss three
mechanisms that might underlie the beneficial effect of taurine in heart f
ailure. First, taurine promotes natriuresis and diuresis, presumably throug
h its osmoregulatory activity in the kidney, its modulation of atrial natri
uretic factor secretion and its putative regulation of vasopressin release.
However, it remains to be determined whether taurine treatment promotes sa
lt and water excretion in humans with heart failure. Second, taurine mediat
es a modest positive inotropic effect by regulating [Na+](i) and Na+/Ca2+ e
xchanger flux. Although this effect of taurine has not been examined in hum
an tissue, it is significant that it bypasses the major calcium transport d
efects found in the failing human heart. Third, taurine attenuates the acti
ons of angiotensin II on Ca2+ transport, protein synthesis and angiotensin
II signaling. Through this mechanism taurine would be expected to minimize
many of the adverse actions of angiotensin II, including the induction of c
ardiac hypertrophy, volume overload and myocardial remodeling. Since the AC
E inhibitors are the mainstay in the treatment of congestive heart failure,
this action of taurine is probably very important.