Abstract
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.
Keywords: Sulphur-containing amino acids, taurine, cysteine, catecholamines, cardiotoxicity, arrhythmias, oxidative damage, heart function.
Current Medicinal Chemistry
Title:Potential of Sulphur-containing Amino Acids in the Prevention of Catecholamine-induced Arrhythmias
Volume: 25 Issue: 3
Author(s): Adriana Adameova *, Paramjit S. Tappia, Robert Hatala and Naranjan S. Dhalla
Affiliation:
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, Bratislava,Slovakia
Keywords: Sulphur-containing amino acids, taurine, cysteine, catecholamines, cardiotoxicity, arrhythmias, oxidative damage, heart function.
Abstract: 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.
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Cite this article as:
Adameova Adriana *, Tappia S. Paramjit , Hatala Robert and Dhalla S. Naranjan, Potential of Sulphur-containing Amino Acids in the Prevention of Catecholamine-induced Arrhythmias, Current Medicinal Chemistry 2018; 25 (3) . https://dx.doi.org/10.2174/0929867324666170526121726
DOI https://dx.doi.org/10.2174/0929867324666170526121726 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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