Essay On Describe The Generation Of An Action Potential In Smooth And Cardiac Muscle Notes

Describe the generation of an action potential in smooth and cardiac muscle

The cardiac muscle is myogenic as it can generate its own action potential at a constant rate which leads to the heart pumping in a regular rhythm. The cardiac action potential originates in a specialised knot of myocytes known as the sinoatrial node which is found in the right atrium at the upper end of the crista terminalis. In these myocytes the membrane potential depolarises spontaneously and once threshold is reached an action potential is generated which propagates to other myocytes within the heart which are connected by gap junctions. As the SAN is responsible for generating the action potential at a regular rate of about 60-100 beats per minute it is often referred to as the pacemaker, however its activity can be modulated by inputs of the autonomic nervous sytem; the vagus nerve decreases the heart rate whereas sympathetic nerves increase the heart rate. Once the action potential is generated in the SAN it is then propagated to the right and then the left atrium within about 40ms. The impulse is then propagated to the atrio-ventricular node which is found in the base of the right atrium. The impulse is prevented from spreading to the ventricles due to the atrioventricular ring made of non conduction fibrous tissue. In order for the impulses to reach the ventricles the impulses are propagated through the atrioventricular bundle of HIS which originates from AV node and divides into a left and right branch either side of the interventricular septum. This bundle then terminates as purkinje fibres which conduct action potential to the ventricular myocytes and causes simulataneous contraction in both ventricles from the apex upwards.

The action potentials generated in different regions of the heart vary in their initiation time, shape and duration. This occurs because the heart is a heterogenous organ where the myocytes in different regions are specialised for specific functions and this results in the cells having a differing permeability to different ions due to them having a distinct set of ion channels. Another factor affecting action potential is that different regions of the heart have differing membrane capacitance. Myocytes that are found in the SAN, AVN are specialised in generating action potentials, whereas atrial and ventricular myocytes are specialised in conduction and the myocytes that make up the bundle of his and purkinje fibres are specialised in conducting the impulses.

Sino-atrial node

The heart has three intrinsic pacemaking tissues which are the SA, AV nodes and the purkinje fibres. The key function of these tissues is to spontaneously depolarise the membrane to threshold and generate action potentials at a regular rhythm. The primary pacemaker is the SAN node as it generates the highest frequency of action potentials and it is these that are propagated around the heart. However if the myocytes in the SAN are damaged, the role of setting the heart rate is taken over by the AVN node.

The maximum diastolic potential that occurs during phase 4 (occurs after repolarisation) is roughly between -60mv and -70mv. In comparison to the atrial and ventricular myocytes the resting membrane potential is less negative and this is due to the large influx of sodium ions through the sodium ion channels. However the resting membrane potential is not stable and it gradually depolarises to a threshold of about -55mv. The main reason why the membrane potential is not stable is that SAN cells lack the background potassium conductance which stabalises the Em in other cells. Also contributing to the depolarisation is the pacemaker current. The pacemaker current consists of the following things:

• An influx of calcium ions through T type voltage gated calcium channels which are open at resting membrane potentials. The evidence that this type of channel contributed to the depolarising current was shown using ethosuximide which it a T type Calcium channel blocker. The drug resulted in a decrease in the pre-potential slope

• Na-Ca exchange current- when calcium ion concentrations increase due to the influx through T type voltage gated calcium ion channels, Na-Ca translocase is activated which pumps 1 calcium out of the myocyte in exchange for 3 Na+ into the cell. This results in a net positive charge entering the cell and contributes to the depolarisation

• Funny current- This is caused by the opening of a nonspecific cation channel which is activated at negative diastolic potentials and is called hyperpolarisation activated cyclic nucleotide. These channels conduct both potassium and sodium and leads to an inward depolarising current. The presence of the funny current was shown using ivabradine which is an inhibitor of the funny current and is used to slow the heart rate therapeutically.

• De activation of the potassium current- as phase three hyperpolarisation ends the voltage gated potassium ion channels slowly close and this leads to a decrease in the outward current causing the membrane potential to become more and more depolarised over time

The combination of all these currents forms the pacemaker current which is a net inward current that causes the membrane potential to eventually reach threshold. Once threshold is reached L type voltage gated calcium ion channels open and this leads to the influx of calcium ions which leads to further depolarisation. In comparison to the action potentials that occur in the ventricles and atria the action potentials formed in the SAN have slow upstrokes. This is because SAN don’t have voltage gated sodium ion channels and the voltage gated calcium channels that cause the action potential have very slow kinetics. The smaller calcium current that...

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