The Cardiac Transmembrane potential Dependends mainly on k, Nat, and ca Each phase of the action potential is associated with a change in conductance to one or more ions The Resting Potential Is Determined by lonic Diffusion A K K 150 mEg/L 5 mEg/L Electrostatic Chemical 615log(K+/K+1
The Cardiac Transmembrane Potential Dependends Mainly on K+ , Na+ , and Ca++ Each phase of the action potential is associated with a change in conductance to one or more ions. The Resting Potential Is Determined by Ionic Diffusion
After raising Ko, the measured value of vm approximates that predicated by the Nernst equation for Km(equilibrium potential). The measured values are slightly less negative than those predicted by Nernst equation because of the small but finite gN IIII External K concentration(mM) Figure 17-3 The Vm of a cardiac muscle fiber varies inversely with the K concentration of the external medium. The oblique blue line represents the E predicted by y the Nernst equation
After raising [K]o, the measured value of Vm approximates that predicated by the Nernst equeation for Km (equilibrium potential). The measured values are slightly less negative than those predicted by Nernst equation because of the small but finite gNa
The Fast response Depends on Nat Phase o is genesis of the upstroke Any stimulus that abruptly changes the resting membrane potential to a critical value A ( called the threshold阈值) results in an action potential lonic The rapid depolarization B (phase O)is related almost exclusively to the influx of Nat into the myocyte due to a sudden FIGURE 16-9. Changes in gNa gca, and gk during phases 0 to 4 of the action potential (A)of a fast-response cardiac cell. The conductance diagrams(B)are qualita increase in gNa. tive, not quantitative
The Fast Response Depends on Na+ Phase 0 is genesis of the upstroke Any stimulus that abruptly changes the resting membrane potential to a critical value (called the threshold 阈值) results in an action potential. The rapid depolarization (phase 0) is related almost exclusively to the influx of Na+ into the myocyte due to a sudden increase in gNa
The amplitude of the action potential (the potential change during phase o)varies linearly with the logarithm of INato When Nato is increased E-20 from about 20% ofits normal value to about 150% of its normal value, the transmembrane potential at Resting membrane the peak of the action potential increases from 8101520 100150 about -20 mv to about +40 External Na* concentration(% of normall FIGURE 16-7. The [Na'l in the external medium is m
When [Na+ ]o is increased from about 20% of its normal value to about 150% of its normal value, the transmembrane potential at the peak of the action potential increases from about -20 mV to about +40 mV. The amplitude of the action potential (the potential change during phase 0) varies linearly with the logarithm of [Na+ ]o
When the resting membrane potential, vm, is suddenly changed from -90 mv to the threshold level of about -65 mv the properties of the cell membrane change dramatically Nat enters the myocyte Action through specific fast Na channels that exist in the membrane conductances These channels can be blocked by the puffer fish toxin, tetrodotoxin FIGURE 16-9. Changes in gNa gca, and gx during phases o to 4 of the action potential (A)of a fast-response cardiac cell. The conductance diagrams(B)are qualita tive, not quantitative
When the resting membrane potential, Vm, is suddenly changed from -90 mV to the threshold level of about -65 mV the properties of the cell membrane change dramatically. Na+ enters the myocyte through specific fast Na+ channels that exist in the membrane. These channels can be blocked by the puffer fish toxin, tetrodotoxin