A typical transmembrane action potential recorded from an SA node cell is depicted in
Fig. 16.10B.
In comparison with the transmembrane potential recorded from a ventricular myocardial cell (see
Fig. 16.10A ), the resting potential of the SA node cell is usually less negative, the upstroke of the action potential (phase 0) is less steep, the plateau is not sustained, and repolarization (phase 3) is more gradual. These are characteristic attributes of the slow response. Tetrodotoxin (which blocks the fast Na+ current) has no influence on the SA nodal action potential because the action potential upstroke is not produced by an inward Na+ current through fast channels. Thus tetrodotoxin has no effect on cells that exhibit the slow response.
Ordinarily,thefrequencyofpacemakerfiringiscontrolled system.Increasedsympatheticnervousactivity,throughthe releaseofnorepinephrine,raisestheheartrateprincipallyby increasingtheslopeoftheslowdiastolicdepolarization.Thismechanismofincreasingheartratefunctionsduringphysical exertion,anxiety,orcertainillnessessuchasfebrileinfectiousA diseases.Increasedvagalactivity,throughthereleaseof acetylcholine,diminishestheheartratebyhyperpolarizingthepacemakercellmembraneandreducingtheslope oftheslowdiastolicdepolarization.Thesemechanisms predominantoversympatheticactivity.Anextremeexample isvasovagalsyncope,abriefperiodoflightheadednessorlossofconsciousnesscausedbyanintenseburstofvagal activity.Thistypeofsyncopeisareflexresponsetopainor tocertainpsychologicalstimuli.
•Fig. 16.18 Mechanisms Involved in the Changes in Frequency of Pacemaker Firing. A, Areductionintheslope(fromwaveatowave b)ofslowdiastolicdepolarizationdiminishesthefiringfrequency.TP,thresholdpotential.B, Anincreaseinthethresholdpotential(fromTP-1toTP-2)oranincreaseinthemagnitudeofthemaximumdiastolicpotential(fromwavesegmentsatod)alsodiminishesthefiringfrequency.(FromHoffmanBF,CranefieldPF.Electrophysiology of the Heart. NewYork:McGraw-Hill;1960.)
The transmembrane potential during phase 4 is much less negative in SA (and AV) nodal automatic cells than in atrial or ventricular myocytes because nodal cells lack the iK1 (inward rectifying) type of potassium channel. Thus the ratio of gK to gNa during phase 4 is much less in nodal cells than in myocytes. Hence, during phase 4, Vm deviates much more from the K+ Nernst equilibrium potential (EK) in nodal cells than it does in myocytes.
The principal feature of a pacemaker cell that distinguishes it from the other cells manifests in phase 4. In nonautomatic cells, the potential remains constant during this phase, whereas a pacemaker fiber is characterized by slow diastolic depolarization throughout phase 4. Depolarization proceeds at a steady rate until a threshold is attained, and an action potential is then triggered.
Pacemaker cell frequency may be varied by a change in (1) the rate of depolarization during phase 4, (2) the maximal negativity during phase 4, or (3) the threshold potential (
Fig. 16.18). When the rate of slow diastolic depolarization is increased, the threshold potential is attained earlier, and the heart rate increases. A rise in the threshold potential delays the onset of phase 0, and the heart rate is reduced. Similarly, when the maximal negative potential is increased, more time is required to reach the threshold potential, when the slope of phase 4 remains unchanged, and the heart rate therefore diminishes.
Ionic Basis of Automaticity
Several ionic currents contribute to the slow diastolic depolarization that characteristically occurs in the automatic