Plateau phase of ventricular muscle is d/f opening of

C i.e. Ca++-Nat Channel In cardiac (e.g. ventricular) muscle, rapid depolarization phase (0) is d/t Nat influx through rapidly opening fast Nat channels (Nat current, INa); initial rapid repolarization phase (1) is d/t inactivation of Nat channel; platue phase (2) is d/t Cattinflux (Ca+tcurrent, Ica) through more slowly opening (slow) Ca++channels (also called calcium-sodium channels) and a slow repolarization phase (3) due to net Kt efflux through multiple types of K+ channels, allows the cell to return to resting membrane potential. Myocardial fibers (cells) have RMP of approximately -90mv. Action Potential in Cardiac Ventricular Muscles volts in ventricular muscle fibers instead of -55 milivolts in the nodal fibers. - Action potential in cardiac muscle fibers averages about 105 mili volts i.e. the intracellular potential rises form a very negative -90 mV between beats to slightly positive +20 mV during each beat. 3 type of membrane ion channels in cardiac muscles responsible for causing the voltage changes include Channel Effect Fast Na' Rapidly opening of fast sodium channels for Channel 10,000 the of a second) causes rapid influx of positive sodium ion (Na+) to the interior of cardiac muscle fiber (Necurrent, IN.). It is responsible for rapid upstroke spike of action potential or rapid depolarization phase 0. Initial rapid repolarization phase lis caused by inactivation of Na+ channels. Slow Ca++ Slower opening of slow calcium (or sodium? (Na+ - Ca++) calcium) channels for about 0.3 second (i.e Channels longer duration) causes large influx of both Ca*+ and Na+ positive ions to interior of cardiac muscle fibre. This (Ca++ current/influx, Ica mainly) is responsible for maintenance of prolonged period of depolarization or platue phase (2) of ventricular AP. Potassium Rapid diffusion of large amounts of positive K+ (K+) Channels ions in outward direction (efflux) from the cardiac muscle fibre (Ek+, K+ current) immediately returns the membrane potential to its resting levels, thus ending the AP Difference b/w AP of Cardiac of Skeletal Muscles Cardiac muscles have prolonged AP (Action potential) and a platue phase, whereas skeletal muscles do not because AP of skeletal muscle is caused and almost entirely by sudden opening of fast Na+ channels for a very sho period. At the end of this abrupt closure, repolarization occurs and AP is over in another thousandth of a second. Whereas AP in cardiac muscle is caused by same fast Na+ channels as well as slow Ca+ (Na+ - channels which are slower to open and more impoantly remain open for several tenths of a second (i.e prolonged duration) thereby maintaining prolonged period of depolarization, causing the platue phase. In skeletal muscles, Ca++ ions for contraction is derived from intracellular sacroplasmic reticulum. Whereas, in cardiac muscles the Ca** that enters during plate phase activate the muscle contractile process. Immediately after the onset of AP, the permeability of cardiac muscle fiber for K+ decreases about 5 folds as a result of excess Ca++ influx through Ca++ channels. Therefore, greatly decreased outflux of positively charged K+ ions during AP platue in cardiac muscles prevents early return of AP voltage to its resting levels. This greatly decreased K+ permeability is not seen in skeletal muscles. Difference b/w AP of Cardiac Muscle & Sinus Nodal Fibers - AT the less negative (- 55 mV) RMP of nodal fibers the fast Na* channels mainly have already become inactivated (or blocked). Therefore only the slow Na+ channels can become activated (open) and cause AP. - So AP is slower to develop in nodal fibers than ventricular fibers. Similarly return of potential to its negative resting state occurs slowly as well rather than the abrupt return that occurs in ventricular muscles.