Ventricular depolarization takes longer because impulses in the left ventricle must travel from cell to cell rather than traveling down the left bundle branch and Purkinje fibers.
(This will lead to a longer QRS complex on an ECG)
Myocardial contraction
Myocardial cells can generate action potentials spontaneously due to the presence of funny (If) channels that allow for a slow influx of sodium ions, as well as T-type calcium channels that contribute to the depolarization phase of the action potential. These channels, coupled with the unique organization of ion channels in the myocardial cell membrane, enable automaticity in these cells.
Class I antiarrhythmic drugs work by inhibiting the sodium channel. Class IA agents work by inhibiting open voltage-dependent Na+ channels. This will slow phase 0 and increase the length of the effective refractory period. Its effect is dependent on frequency. The drugs dissociate slowly from closed channels so when the frequency of the action potential is high, the drug can prevent the the Na+ channel from contributing to the action potential as it is still there. One example of a class IA agent is the procainamide which is used to treat ventricular arrhythmias when administered intravenously. Class IB agents work by blocking closed voltage-dependent Na+ channels. It is often used to treat ventricular arrhythmia after an acute myocardial infarction. An acute myocardial infarction often leads to anoxia so many Na+ channels will be inactiated and closed. These Na+ channels are hence susceptible to class IB agents. An example of a class IB agent is the lidocaine. Class III antiarrhythmic drugs work by blockign the outward K+ currents. This leads to the action potential belong prolonged. The QT interval will increase the the effective refractory period will also increase. One example of class III antiarrhythmic drug is the amiodarone. It inhibits the K+ channel, the inactivated Na+ channel, and the beta adrenoceptors.
It creates an action potential
No, hyperpolarization graded potentials do not lead to action potentials. Hyperpolarization makes the membrane potential more negative, which inhibits the generation of an action potential by increasing the distance from the threshold potential needed to trigger an action potential.
It simulates the node, which then sends impulses to the AV node, which disperses these impulses through the cardiac muscle to cause a cardiac cycle (rhythmic beating and relaxing of atria and ventricles)
The regeneration of action potential is called "propagation." It involves the transmission of the action potential along the length of the neuron's axon.
Curare does NOT create an action potential. It binds to nicotinic acetylcholine receptors (which are primarily excitatory), and prevents the formation of an action potential.
action potential
It doesn't. I prevents an action potential from forming.
Action potential
No, subthreshold stimulation is not sufficient to trigger an action potential. The membrane potential needs to reach a certain threshold level for an action potential to be generated. Subthreshold stimulation only produces graded potentials that do not reach the threshold for firing an action potential.