Abstract
The sinoatrail node (SAN), the dominant pacemaker in the heart, was originally described by Keith et al. in 1907 [1]. The SAN is a subepicardial structure located at the junction of the right atrium and the superior vena cava [1]. The SAN spontaneous firing activity is not completely understood. Two predominant mechanisms are proposed to serve as the initiation of the sinus activity: The If channels (sodium and potassium ionic currents) and spontaneous intracellular calcium released by sarcoplasmic reticulum [2]. These two mechanisms are not mutually exclusive, and current evidence suggests that they may be complementary in their pacemaker actions. The SAN is richly innervated by the autonomic nervous system and the balance between the parasympathetic and sympathetic inputs modulate pacemaker rate. The vagal parasympathetic nerves slow the SAN rate and are dominant at rest, while increased sympathetic nerve traffic as well as adrenal medullary release of catecholamines increase sinus rate during exercise and stress.
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References
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Guzman, J.C., Morillo, C.A. (2015). Sick Sinus Syndrome. In: Alboni, P., Furlan, R. (eds) Vasovagal Syncope. Springer, Cham. https://doi.org/10.1007/978-3-319-09102-0_22
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DOI: https://doi.org/10.1007/978-3-319-09102-0_22
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