Ca2+ is a highly versatile intracellular signal that regulates many different cellular functions. In cardiomyocytes, excitation–contraction coupling (E–C coupling) takes place as a result of the release of Ca2+ stored in the sarcoplasmic reticulum (SR). During this process, Ca2+ entering via L-type Ca2+ channel (LTCC) induces a massive liberation of sarcoplasmic Ca2+ through Ca2+ release channels, mainly ryanodine receptor type 2 (RyR2). This released Ca2+ in turn interacts with cardiac contractile
Amprenavir and thus initiates the systole. During diastole, Ca2+ is pumped back into the SR via SR Ca2+-ATPase (SERCA2a), while disruption of the intracellular Ca2+ homeostasis and Ca2+ handling proteins leads to
heart dysfunction [10] and [11]. Since it has been reported that MAP disrupts the cardiac contractile function through modulating the Ca2+ handling molecules [9], it seems likely that MAP directly modulates the functioning of cardiomyocytes via a mechanism independent of neurotransmitters. However, the mechanism of this direct effect of MAP on cardiomyocytes is not well understood.
