Although many drugs are effective in the acute treatment of arrhythmia, antiarrhythmic prophylaxis is still a major problem in cardiovascular pharmacology because the common antiarrhythmic drugs possess considerable proar-rhythmic risk, especially antiarrhythmics of classes I and III . Thus, there is a need to find new ways and mechanisms of action for antiarrhythmic prophylaxis. We recently reported a reduction of dispersion by a new antiarrhythmic peptide acting on cellular coupling .
In principle there are three possible means of affecting cardiac action potential generation and spread, thereby possibly exerting antiarrhythmic effects: first, transmembrane channels may be blocked by sodium channel blockers (class Ia, Ib, Ic antiarrhythmics), by potassium channel blockers (class III antiarrhythmics) or by calcium antagonists (class IV antiarrhythmics); second, cardiac receptors may be blocked by beta1-adrenoceptors (class II antiarrhythmics) to reduce heart rate; or, third, the intercellular communication may be affected, thereby interfering with the spread of the action potential. Cardiovascular pharmacology in recent years has focused on the development of new blockers of the transmembrane channels.
Cellular coupling, on the other hand, is provided by gap junctional channels, which are hexadimeric channels in the heart consisting of either connexin 40 (atrium and specific conductive system) or connexin 43 (most prominent in the whole heart ). These channels are regulated via cAMP, and by phosphorylation via tyrosine and serine kinases (reviewed in 8,9), by pH at histidine 95 of connexin 43 , by PCO2 , by intracellular calcium concentration and by ATP . Injection of sodium also leads to cellular uncoupling, as shown by DeMello . With these manipulations it is possible to uncouple cells. However, enhancing coupling is problematic. Your turn to find out more about the possibility to get Birth Control Ortho Tri Cyclen click here and pay tons less.