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As an action potential (nerve impulse) travels down an axon there is a change in electric polarity across the membrane of the axon. In response to a signal from another neuron, sodium- (Na +) and potassium- (K +)–gated ion channels open and close as the membrane reaches its threshold potential.
In excitable cells, such as neurons, the delayed counterflow of potassium ions shapes the action potential. By contributing to the regulation of the cardiac action potential duration in cardiac muscle, malfunction of potassium channels may cause life-threatening arrhythmias. Potassium channels may also be involved in maintaining vascular tone.
Figure 3 shows the important ion channels involved in the cardiac action potential, the current (ions) that flows through the channels, their main protein subunits (building blocks of the channel), some of their controlling genes that code for their structure, and the phases that are active during the cardiac action potential.
Potassium channel blockers exhibit reverse use-dependent prolongation of the action potential duration. Reverse use dependence is the effect where the efficacy of the drug is reduced after repeated use of the tissue. [11] This contrasts with (ordinary) use dependence, where the efficacy of the drug is increased after repeated use of the tissue.
This combination of closed sodium channels and open potassium channels leads to the neuron re-polarizing and becoming negative again. The neuron continues to re-polarize until the cell reaches ~ –75 mV, [2] which is the equilibrium potential of potassium ions. This is the point at which the neuron is hyperpolarized, between –70 mV and –75 mV.
However this G-protein works by inhibiting, the cAMP pathway, therefore, preventing the sympathetic nervous system from increasing heart rate. As well as this, in the SAN, the G-protein activates specific potassium channel, that opposes action potential initiation (see SAN for more details), thus slowing heart rate. [2]
The potassium channels exhibit a delayed reaction to the membrane repolarisation, and, even after the resting potential is achieved, some potassium continues to flow out, resulting in an intracellular fluid that is more negative than the resting potential, and during which no action potential can begin (undershoot phase/refractory period). This ...
At this point, the calcium ion channels close and potassium channels open, allowing outflux of K + and resulting in repolarization. When the membrane potential reaches approximately −60 mV, the K + channels close and Na + channels open, and the prepotential phase begins again. This process gives the autorhythmicity to cardiac muscle.