SA node Action Potential Normally the pacemaker cells of the SA node has a resting membrane potential of - 60 millivolts.

At this potentials channels called If channels (Funny channels) or HCN (hyperpol arization activated secret nucleotide channels) which are actually Na/K channels (they allow more sodium to enter the cells and less potassium to exit the cells ) allow a net influx of sodium into the cells. The influx of sodium into the cells carries with it positive charge which causes the membrane potential to reach a threshold of around -45 millivolts. This even t closes the If channels and triggers the opening of another type of channel cal led the T-type Ca channels. (T stands for transient calcium channels because the y open for a very short time). The influx of calcium carries with it positive ch arge which causes the membrane potential to reach a threshold of -30 millivolts which is the threshold for opening L-type Calcium channels. This event causes th e T-type calcium channels to close and for the L-type Calcium channels to open. These are the main voltage gated channels in the pacemaker cells. Which allows m ore calcium ions to enter the cells. (L stands for long because the opening time for these channels is longer and slower to open and close). The large influx o f calcium ions brought about by the opening of the L-type calcium channels cause s the membrane potential to spike up to 0 millivolts. At this point the L type calcium channels will close. And the voltage gated pota ssium channels or the calcium dependent potassium channels will open and potassi um leaves the cell (efflux) carrying with it positive charge which cause the mem brane potential to go back to below -45 millivots. This will again reopen the If channels and sodium will again enter the cell. And the process repeats itself. The If channels are the ones responsible for the pacemaker activity of the SA no de because the open and close periodically without any external help as long as the membrane potential goes below -45 millivolts. Cardiac Myocyte Action Potential This graph shows the action potential in non pace maker cells or the cardiac myo cytes in the atria and ventricles. Unlike the resting membrane potential of the pacemaker cells, the resting membra ne potential for non pacemaker cells is -80 millivolts because they are more lea ky to potassium. The cardiac myocytes are connected by gap junctions to allow the wave of depolar ization to travel from cell to cell through the gap junctions. From pacemaker ce lls the action potential reaches the cardiac myocytes. If an action potential was generated by the pacemaker cells, the wave of depolar ization passes through the gap junctions and causes the resting membrane potenti al of non pacemaker cells (-80 millivolts) to increase until it reaches a thresh old of around -70 millivolts. This causes voltage gated sodium channels to open causing the large influx of sodium into the cardiac myocytes which carries with it positive charge causing rapid depolarization of the cell. This is seen as the upward spiking in the graph. This is responsible for the generation of these "f ast-response" action potentials. Once it reaches positive the fast sodium chan nels close. An initial repolarization that is caused by the opening of a special type of transient outward K+channel is seen. This causes a short-lived, hyperpo larizing outward K+ current and a dip in the graph. However, because of the larg e increase in slow inward gCa++ occurring at the same time and the transient nat ure of IKto, the repolarization is delayed and there is a plateau phase in the a ction potential (phase 2). This inward calcium movement is through long-lasting (L-type) calcium channels that open up when the membrane potential depolarizes t o about -40 mV. This plateau phase prolongs the action potential duration and di stinguishes cardiac action potentials from the much shorter action potentials fo und in nerves and skeletal muscle. Repolarization (phase 3) occurs when gK+ (and therefore IK) increases, along with the inactivation of Ca++ channels (decrease d gCa++). Therefore, the action potential in non-pacemaker cells is primarily determined b y relative changes in fast Na+, slow Ca++ and K+conductances and currents.