Differences Between Physiological and Pharmacological Actions of Taurine.

In many experimental studies, pharmacological levels of taurine have been used to study physiological functions of taurine. However, this approach is unlikely to be fruitful, as pharmacological administration increases extracellular taurine, while physiological actions of taurine require alterations in intracellular taurine. Recognizing that different mechanisms might underlie the pharmacological and physiological actions of taurine, cardiac properties before and after exposure to various extracellular or intracellular concentrations of taurine were examined. To assess the effect of physiological taurine, myocardial contractility and metabolic status were compared in hearts containing different intracellular taurine concentrations. By contrast, the pharmacological actions of taurine were assessed in normal hearts perfused with buffer containing or lacking 10 mM taurine. Both pharmacological and physiological taurine increased contractile function and oxygen consumption. Yet, the pharmacological actions of taurine on contractile function were dependent on the L-type Ca2+ channel, while the sarcoplasmic reticular Ca2+ ATPase contributed to the physiological actions of taurine. ATP generation from available substrates, glucose, fatty acids, and acetate was increased for both the physiological and pharmacological actions of taurine. However, taurine supplementation enhanced ATP generation by elevating respiratory chain complex I activity and by stimulating metabolic flux through reductions in the NADH/NAD+ ratio, while the pharmacological actions of taurine can be traced to elevations in [Ca2+]i and the observed positive inotropic effect. Thus, the mechanisms underlying the pharmacological actions of taurine on contractile function and energy metabolism are entirely different than those contributing to the physiological actions of taurine.

The Role of Taurine in Mitochondria Health: More Than Just an Antioxidant.

Taurine is a naturally occurring sulfur-containing amino acid that is found abundantly in excitatory tissues, such as the heart, brain, retina and skeletal muscles. Taurine was first isolated in the 1800s, but not much was known about this molecule until the 1990s. In 1985, taurine was first approved as the treatment among heart failure patients in Japan. Accumulating studies have shown that taurine supplementation also protects against pathologies associated with mitochondrial defects, such as aging, mitochondrial diseases, metabolic syndrome, cancer, cardiovascular diseases and neurological disorders. In this review, we will provide a general overview on the mitochondria biology and the consequence of mitochondrial defects in pathologies. Then, we will discuss the antioxidant action of taurine, particularly in relation to the maintenance of mitochondria function. We will also describe several reported studies on the current use of taurine supplementation in several mitochondria-associated pathologies in humans.

Inhibition of angiotensin II-induced hypertrophy and cardiac dysfunction by North American ginseng (Panax quinquefolius).

We determined whether North American ginseng (Panax quinquefolius L.) mitigates the effect of angiotensin II on hypertrophy and heart failure. Angiotensin II (0.3 mg/kg) was administered to rats for 2 or 4 weeks in the presence or absence of ginseng pretreatment. The effect of ginseng (10 µg/mL) on angiotensin II (100 nM) - induced hypertrophy was also determined in neonatal rat ventricular myocytes. We also determined effects of ginseng on fatty acid and glucose oxidation by measuring gene and protein expression levels of key factors. Angiotensin II treatment for 2 and 4 weeks induced cardiac hypertrophy as evidenced by increased heart weights, as well as the upregulation of the hypertrophy-related fetal gene expression levels, with all effects being abolished by ginseng. Ginseng also reduced abnormalities in left ventricular function as well as the angiotensin II-induced increased blood pressure. In myocytes, ginseng abolished the hypertrophic response to angiotensin II as assessed by surface area and gene expression of molecular markers of hypertrophy. Ginseng modulated angiotensin II-induced abnormalities in gene expression and protein levels of CD36, CPT1M, Glut4, and PDK4 in vivo and in vitro. In conclusion, ginseng suppresses angiotensin II-induced cardiac hypertrophy and dysfunction which is related to normalization of fatty acid and glucose oxidation.