Apico-basal inhomogeneity in distribution of ion channels in canine and human ventricular myocardium

Department of Physiology, University of Debrecen, P.O. Box 22, H-4012 Debrecen, Hungary.
Cardiovascular Research (Impact Factor: 5.94). 04/2005; 65(4):851-60. DOI: 10.1016/j.cardiores.2004.11.022
Source: PubMed


The aim of the present study was to compare the apico-basal distribution of ion currents and the underlying ion channel proteins in canine and human ventricular myocardium.
Ion currents and action potentials were recorded in canine cardiomyocytes, isolated from both apical and basal regions of the heart, using whole-cell voltage clamp techniques. Density of channel proteins in canine and human ventricular myocardium was determined by Western blotting.
Action potential duration was shorter and the magnitude of phase-1 repolarization was significantly higher in apical than basal canine myocytes. No differences were observed in other parameters of the action potential or cell capacitance. Amplitude of the transient outward K(+) current (29.6+/-5.7 versus 16.5+/-4.4 pA/pF at +65 mV) and the slow component of the delayed rectifier K(+) current (5.61+/-0.43 versus 2.14+/-0.18 pA/pF at +50 mV) were significantly larger in apical than in basal myocytes. Densities of the inward rectifier K(+) current, rapid delayed rectifier K(+) current, and L-type Ca(2+) current were similar in myocytes of apical and basal origin. Apico-basal differences were found in the expression of only those channel proteins which are involved in mediation of the transient outward K(+) current and the slow delayed rectifier K(+) current: expression of Kv1.4, KChIP2, KvLQT1 and MinK was significantly higher in apical than in basal myocardium in both canine and human hearts.
The results suggest that marked apico-basal electrical inhomogeneity exists in the canine-and probably in the human-ventricular myocardium, which may result in increased dispersion, and therefore, cannot be ignored when interpreting ECG recordings, pathological alterations, or drug effects.

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    Computing in Cardiology; 09/2014
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    • "Kir2.2, and Kir2.3) ion channels (Karle et al. 2002; Marban 2002; Rook 2007). Earlier, the asymmetrical distribution and apico-basal inhomogeneity of Kir ion channels were investigated by Szabó et al. (2005) and Szentadrassy et al. (2005). They found that there are no transmural differences, at the protein level, in Kir2.1 channels in human and dog ventricles. "
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    • "TTX-sensitive Ca2+ current components have been identified in cardiac tissues under pathological conditions, such as in hypertrophied guinea pig or infarcted rat hearts [4,5]. TTX was shown to block L-type Ca2+ current in ventricular cardiomyocytes isolated from healthy dogs [6], i.e., in a preparation having electrophysiological properties most similar to those of human ventricular myocardium regarding the distribution and kinetic properties of transmembrane ion currents [7,8]. "
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