Background: Various physiological and pathological stimuli can hypersensitize the
sympathetic nervous system resulting in a substantial release of catecholamines (CA) and consequent
alterations in excitation-contraction coupling and excitation-transcription coupling.
Observations: It has been shown that oxidation products of CA, rather than CA themselves, are
responsible for such adaptation to a new equilibrium. While chronic, sustained accumulation of
CA and their toxic products are associated with the depression in cardiac contractile force and
remodeling, acute excessive release of CA can result in brief oxidative bursts and serious damage
leading in lethal arrhythmias. In response to such oxidative stress, dysregulation of ion homeostasis,
activation of neurohumoral system, immune and inflammatory responses, are augmented.
These events are inter-related, and as a complex promote electrical instability. Likewise,
remodeling occurring after the loss of cardiomyocytes, induces the development of a proarrhythmogenic
environment. Thus, CA oxidation products may be involved in triggering arrhythmias
as a result of both changes in cardiac cell automaticity and conduction velocity. In
contrast, sulphur-containing amino acids (S-AA), in particular taurine and its precursor cysteine
have been shown to modulate redox state of the heart. However, the multiple anti-oxidant properties
of S-AA are unlikely to be exclusively responsible for their anti-arrhythmic action. They
also possess additional cytoprotective effects which can stabilize electrical activity of the heart.
Conclusion: It is concluded that specific S-AA may attenuate deleterious effects of supraphysiological
levels of CA and this could serve as an important mechanism for the treatment and/or
prevention of arrhythmogenesis.