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CHAPTER 1 / Cardiac Anatomy and Physiology 23

Table 1-4 ■ CARDIAC IONIC CURRENTS
Current * Charge Carrier Activation Mechanism Function
Inward Currents
Na Voltage AP upstroke
I Na
I Ca (I Si, I Caf , I Cas ) Ca 2 Voltage AP plateau
E–C coupling
AP upstroke
Sinus pacemaker

I f (I h ) Na and K Voltage Spontaneous depolarization
2

I ti (I t’ , I Na, K ) Na and K ?[(Ca ] i After-depolarization
Outward Currents

I K (I x , I x1 , I x2 ) K (Na ) Voltage Repolarization
2
K Voltage, ?[Ca ] Early repolarization
I to
K Voltage Resting potential
I K1
Repolarization
?Plateau potential
K 2 Repolarization
I K Ca [Ca ] i
K ACh, ? voltage Inhibition
I K Ach
Pump/Exchange Currents

Na , K [K ], [Na ] Na –K –ATPase pump
I p

2
Na , Ca 2 [Ca ], [Na ] Na –Ca 2 exchange
I Na, Ca
Background Currents
Na ? Inward leakage
I b Na
Ca 2 ? ? Inward leakage
I b Ca
Cl – ? ?
? I b Cl
*
Currents identified in multicellular preparations are labeled I and currents identified in single-cell preparations are labeled i. Some of these currents are speculative (see text).
Ach, acetylcholine; AP, action potential; E–C, excitation–contraction; [ ], concentration of ion indicated.
Adapted from Brown, H. F. (1982). Electrophysiology of the sinoatrial node. Physiology Review, 62(2), 505–530; Nobel, D. (1981). The surprising heart. Journal of Physiology, 353,
43; Opie, L. (1984). The heart (p. 47). Orlando: Grune & Stratton; and Reuter, H. (1984). Ion channels in cardiac cell membranes. Annual Review of Physiology, 46, 474.
Inward Currents tial and rate of stimulation. Organic dihydropyridines, such as
nifedipine, also block this channel.
The inward currents are carried by sodium or calcium ions mov-
ing into the cell. For each ion, there are several different types of Pacemaker Current
channels, each with its own gating characteristics.
Pacemaking results from the combination of at least four currents.
There is a time-dependent inactivation of the potassium current,
Fast Inward Current I NA
and thus a loss of outward current (which would tend to hyper-
The fast sodium current is activated to cause rapid depolarization
polarize). This inactivation alone does not produce depolariza-
in phase 0 of fast-response cells. It was discussed in some detail
tion; channels that carry ions with an equilibrium potential posi-
previously. Briefly, the sodium channel opens with depolarization
tive to the membrane potential also must open. The currents
to threshold ( 70 to 60 mV), but quickly closes because of in-
involved are I h , I Ca , and background sodium current. I h channels
activation. Repolarization is necessary to remove the inactiva-
38
tion. The fast sodium current is blocked by the puffer fish poi- open at negative (hyperpolarized) potentials (hence the designa-
tion “h”), close at positive potentials, and allow passage of both
son tetrodotoxin. Many antiarrhythmic agents, particularly class I
sodium (hence a depolarizing influence) and potassium. Gating is
agents, alter this current.
slow. Similarly, a sodium leak current occurs and is a depolarizing
Calcium Currents influence. Calcium channels are activated with depolarization.
With increasing depolarization, the calcium T channels open, car-
The two major types of calcium channels are termed L (long-last-
rying inward depolarizing calcium current (I Ca ). 42
ing) and T (transient). The L current activates with depolariza-
tions beyond –40 mV and then slowly inactivates. The T current
activates at –70 mV and rapidly diminishes. Both channels prob- Transient Diastolic Inward Current I ti
ably contribute to maintaining the plateau phase of the cardiac ac- The transient diastolic inward current is a nonselective current
tion potential. The T channels contribute to spontaneous depo- that carries both sodium and potassium and may be activated by
larization in pacemaker cells and the L channels contribute to the intracellular calcium. It is not normally active but may be in-
action potential upstroke in these cells. These currents may be po- volved in initiating delayed depolarizations and triggering ar-
tentiated by -adrenergic (catecholamine) stimulation and dimin- rhythmias in Purkinje and ventricular muscle cells, particularly
ished by acetylcholine and acidosis. 36 The current is blocked by when extracellular potassium concentration is low. Other inward
inorganic compounds such as lanthanum, cobalt, nickel, and currents have been identified. Sodium and calcium “leak” currents
manganese. Organic charged tertiary amines, such as verapamil, and the sodium–calcium exchange mechanisms can generate
block the slow channel. The block depends on membrane poten- small inward currents.