The formation of ectopic pacemakers and a partial block of impulse conduction between cells have also been reported to be involved in the system Dub inhibitors of aconitine induced fibrillation. The very first flutter is established at the stage of acceleration in ectopic pacemaker exercise, as time progresses the flutter then changes spontaneously to fibrillation. It is possible that these processes are stimulated by the progressive intracellular Ca2 overload since aconitine raises inflow of Na ions to the cell, induced by the reversed mode of Na Ca2 exchange exercise. For that reason, often a partial or complete block of impulse transmission connected with aconitine toxicity is caused by a disorder of the gap junction, because the Ca2 ion is a major factor proven to weaken gap junction communication due to a closure of the gap junction channel or due to reduced expression of Cx43 in the gap junction by suppressing PKA mediated phosphorylation. At the start of and during fibrillation, the action potentials, with various amplitudes and differentials of rate of rise, show a mingling of electrical activity in a myocyte. Neuroblastoma This suggests that the initiation of fibrillation is brought about by the electrical interaction between neighbouring cells in close proximity together due to a dysfunction of the gap junction. A higher concentration of heptanol completely closes the gap junction channels and completely prevents electric interaction between cells. Furthermore, a higher concentration of heptanol affects Na, E and Ca2 channel activities. In this disorder, the effects of heptanol on the gap junction can’t be found. A low concentration potent c-Met inhibitor of heptanol induces incomplete inhibition of the gap junction channels with no effects on Na, E or Ca2 channel activity, and accelerates electrical interaction between cells. Just because a low concentration of heptanol incredibly increases the generation of fibrillation, unstable function of the gap junction contributes to this generation. An unstable function of the gap junction is induced from the remodelling of connexin. Furthermore, in the present review, the expression of Cx43 at the gap junction was heterogeneous at the start of fibrillation. Such evidence implies that the generation of the fibrillation is caused by a dysfunction of the gap junction, which thus induces a re-entrant world between adjoining cells. Consequently, the facility of the shift from flutter to fibrillation is considered as a sign of the susceptibility of ventricular tissue to fibrillation in relation to the dysfunction of the gap junction. The heart or cardiac muscle strip subjected to hypokalemia is vulnerable to ventricular fibrillation, diabetic or hypertrophic hearts are susceptible to hyperkalemia induced ventricular fibrillation.