Short-Communication: Short-Term Treatment with Taurine Prevents the Development of Cardiac Hypertrophy and Early Death in Hereditary Cardiomyopathy of the Hamster and Is Sex-Dependent.

Premature death due to heart failure is a major health problem. Taurine is a non-essential amino acid that has received much attention. However, although many studies have been carried out on the beneficial effects of taurine in cardiac pathophysiology, no studies have investigated the effect of taurine treatment on the development of hereditary cardiomyopathy (HCM) associated with hypertrophy, heart failure, and early death. This study aims to verify whether short-term treatment (20 days) with taurine in tap water prevents the development of hypertrophy and premature death in hereditary cardiomyopathy of the hamster (HCMH) of the line UM-X7.1 and if its effect is sex-dependent. Our results show that treatment for 20 days with taurine (250 mg/kg/day or 25 mg/animal/day) during the development of the hypertrophic phase (220 days old) significantly decreased (p < 0.01) the heart weight to body weight ratio in male HCMHs without affecting the female. During the 20 days (220−240 days old), there were nearly 40% premature deaths in non-treated males HCMHs and 50% in female HCMHs. Treatment for 20 days wholly and significantly prevented early death in both males and females HCMHs. Our results demonstrate that short-term treatment with taurine prevents the development of cardiac hypertrophy associated with HCM in a sex-dependent manner; however, it prevents early death in a sex-independent fashion. Our results suggest that taurine supplementation could be used to treat HCM.

High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells.

Our knowledge on essential hypertension is vast, and its treatment is well known. Not all hypertensives are salt-sensitive. The available evidence suggests that even normotensive individuals are at high cardiovascular risk and lower survival rate, as blood pressure eventually rises later in life with a high salt diet. In addition, little is known about high sodium (Na+) salt diet-sensitive hypertension. There is no doubt that direct and indirect Na+ transporters, such as the Na/Ca exchanger and the Na/H exchanger, and the Na/K pump could be implicated in the development of high salt-induced hypertension in humans. These mechanisms could be involved following the destruction of the cell membrane glycocalyx and changes in vascular endothelial and smooth muscle cells membranes' permeability and osmolarity. Thus, it is vital to determine the membrane and intracellular mechanisms implicated in this type of hypertension and its treatment.