Biomedical Engineering Reference
In-Depth Information
Table 5.12. Major voltage-gated potassium channels in the heart (Source: [ 466 , 468 ]). Inward-
rectifier (K IR ), voltage-dependent (K V ), and calcium-activated (K Ca )K + channels also regulate the
caliber of arteries and arterioles, especially in the cerebral territory. In the endocardium of human
heart, a small i K , to component with slow recovery kinetics may correspond to K V 1.4 channel.
Several inwardly rectifying currents in mammalian hearts include quasi-instantaneous rectifier i K1 ,
ATP-inhibited i K AT P , and muscarinic receptor-stimulated i K ACh currents through K IR 2.1, K IR 6.2-
SUR1, and G- protein-regulated K IR 3.1-K IR 3.4 (or GIRK1-GIRK4) complexes, res pectively.
Type
Current
Subunits
(Genes)
Ultrarapid delayed rectifier
i K , ur
K V 1.5
(phases 1, 2)
(KCNA5)
Rapid delayed rectifier
i K , r
K V 11.1
(plateau end, phase 3)
(hERG, ERG1, KCNH2)
minK, MiRP1
(KCNE1, KCNE2)
Slow delayed rectifier
i K , s
K V 7.1
(plateau end, phase 3)
(K V LQT1, KCNQ1)
minK
(KCNE1)
Rapid transient outward
i K , to ( r )
K V 4.2/4.3
(phase 1)
(KCND2, KCND3)
KCNIP2
Slow transient outward
i K , to ( s )
K V 1.4
(phases 1, 2)
(KCNA4)
MiRP1
(KCNE2)
Inward rectifier
i K1
K IR
(phase 3, rest)
K IR 2.1
(KCNJ2)
K IR 2.2
(KCNJ12)
The long duration of cardiac action potentials (Sect. 6.5 ) that results from a
coordinated action of numerous channels with diverse properties (gating mode,
activation and inactivation rate, ionic conductance, etc.) is needed to prevent
premature excitation. Three major potassium channels, with a varying concentration
in the sarcolemma according to the transmural location, contribute to ventricular
repolarization: inward rectifier (K IR , i K1 ) that closes during depolarization, rapid
( i K , r )and slow ( i K , s current), delayed rectifiers ,and transient outward K + ( i K , to
current; Table 5.12 ) channels .
The first group of K + channel subunits pertains to the 2TM and 1P class (K 2TM1P )
of inwardly rectifying K + -selective channels K IR 2. i ,K IR 3. i ,andK IR 6. i that cause
 
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