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Cardiac conduction
Stable Identifier
R-HSA-5576891
DOI
10.3180/R-HSA-5576891.1
Type
Pathway
Species
Homo sapiens
ReviewStatus
5/5
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Muscle contraction (Homo sapiens)
Cardiac conduction (Homo sapiens)
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The normal sequence of contraction of atria and ventricles of the heart require activation of groups of cardiac cells. The mechanism must elicit rapid changes in heart rate and respond to changes in autonomic tone. The cardiac action potential controls these functions. Action potentials are generated by the movement of ions through transmembrane ion channels in cardiac cells. Like skeletal myocytes (and axons), in the resting state, a given cardiac myocyte has a negative membrane potential. In both muscle types, after a delay (the absolute refractory period), K+ channels reopen and the resulting flow of K+ out of the cell causes repolarisation. The voltage-gated Ca2+ channels on the cardiac sarcolemma membrane are generally triggered by an influx of Na+ during phase 0 of the action potential. Cardiac muscle cells are so tightly bound that when one of these cells is excited the action potential spreads to all of them. The standard model used to understand the cardiac action potential is the action potential of the ventricular myocyte (Park & Fishman 2011, Grant 2009).
The action potential has 5 phases (numbered 0-4). Phase 4 describes the membrane potential when a cell is not being stimulated. The normal resting potential in the ventricular myocardium is between -85 to -95 mV. The K+ gradient across the cell membrane is the key determinant in the normal resting potential. Phase 0 is the rapid depolarisation phase in which electrical stimulation of a cell opens the closed, fast Na+ channels, causing a large influx of Na+ creating a Na+ current (I
Na+
). This causes depolarisation of the cell. The slope of phase 0 represents the maximum rate of potential change and differs in contractile and pacemaker cells. Phase 1 is the inactivation of the fast Na+ channels. The transient net outward current causing the small downward deflection (the "notch" of the action potetial) is due to the movement of K+ and Cl- ions. In pacemaker cells, this phase is due to rapid K+ efflux and closure of L-type Ca2+ channels. Phase 2 is the plateau phase which is sustained by a balance of Ca2+ influx and K+ efflux. This phase sustains muscle contraction. Phase 3 of the action potential is where a concerted action of two outward delayed currents brings about repolarisation back down to the resting potential (Bartos et al. 2015).
Literature References
PubMed ID
Title
Journal
Year
21357845
The cardiac conduction system
Park, DS
,
Fishman, GI
Circulation
2011
26140724
Ion Channels in the Heart
Grandi, E
,
Ripplinger, CM
,
Bartos, DC
Compr Physiol
2015
19808464
Cardiac ion channels
Grant, AO
Circ Arrhythm Electrophysiol
2009
Participants
Events
Phase 4 - resting membrane potential
(Homo sapiens)
Phase 0 - rapid depolarisation
(Homo sapiens)
Phase 1 - inactivation of fast Na+ channels
(Homo sapiens)
Phase 2 - plateau phase
(Homo sapiens)
Phase 3 - rapid repolarisation
(Homo sapiens)
Ion homeostasis
(Homo sapiens)
Physiological factors
(Homo sapiens)
Participates
as an event of
Muscle contraction (Homo sapiens)
Event Information
Go Biological Process
cardiac conduction (0061337)
Orthologous Events
Cardiac conduction (Bos taurus)
Cardiac conduction (Caenorhabditis elegans)
Cardiac conduction (Canis familiaris)
Cardiac conduction (Danio rerio)
Cardiac conduction (Dictyostelium discoideum)
Cardiac conduction (Drosophila melanogaster)
Cardiac conduction (Gallus gallus)
Cardiac conduction (Mus musculus)
Cardiac conduction (Plasmodium falciparum)
Cardiac conduction (Rattus norvegicus)
Cardiac conduction (Saccharomyces cerevisiae)
Cardiac conduction (Schizosaccharomyces pombe)
Cardiac conduction (Sus scrofa)
Cardiac conduction (Xenopus tropicalis)
Authored
Jassal, B (2014-05-27)
Reviewed
Colotti, G (2015-11-09)
Created
Jassal, B (2014-05-27)
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