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Action potential clamp fingerprints of K+ currents in canine cardiomyocytes: their role in ventricular repolarization.
Acta Physiol (Oxf). 2007 Jul; 190(3):189-98.AP

Abstract

AIM

The aim of the present study was to give a parametric description of the most important K(+) currents flowing during canine ventricular action potential.

METHODS

Inward rectifier K(+) current (I(K1)), rapid delayed rectifier K(+) current (I(Kr)), and transient outward K(+) current (I(to)) were dissected under action potential clamp conditions using BaCl(2), E-4031, and 4-aminopyridine, respectively.

RESULTS

The maximum amplitude of I(to) was 3.0 +/- 0.23 pA/pF and its integral was 29.7 +/- 2.5 fC/pF. The current peaked 4.4 +/- 0.7 ms after the action potential upstroke and rapidly decayed to zero with a time constant of 7.4 +/- 0.6 ms. I(Kr) gradually increased during the plateau, peaked 7 ms before the time of maximum rate of repolarization (V(max)(-)) at -54.2 +/- 1.7 mV, had peak amplitude of 0.62 +/- 0.08 pA/pF, and integral of 57.6 +/- 6.7 fC/pF. I(K1) began to rise from -22.4 +/- 0.8 mV, peaked 1 ms after the time of V(max)(-) at -58.3 +/- 0.6 mV, had peak amplitude of 1.8 +/- 0.1 pA/pF, and integral of 61.6 +/- 6.2 fC/pF. Good correlation was observed between peak I(K1) and V(max)(-) (r = 0.93) but none between I(Kr) and V(max)(-). Neither I(K1) nor I(Kr) was frequency-dependent between 0.2 and 1.66 Hz. Congruently, I(Kr) failed to accumulate in canine myocytes at fast driving rates.

CONCLUSION

Terminal repolarization is dominated by I(K1), but action potential duration is influenced by several ion currents simultaneously. As I(to) was not active during the plateau, and neither I(K1) nor I(Kr) was frequency-dependent, other currents must be responsible for the frequency dependence of action potential duration at normal and slow heart rates in canine ventricular cells.

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Authors+Show Affiliations

Bányász T
Department of Physiology, University of Debrecen, Debrecen, Hungary.
Magyar J
No affiliation info available
Szentandrássy N
No affiliation info available
Horváth B
No affiliation info available
Birinyi P
No affiliation info available
Szentmiklósi J
No affiliation info available
Nánási PP
No affiliation info available

MeSH

Action PotentialsAnimalsCells, CulturedDogsElectrophysiologyFemaleHeart VentriclesMaleMyocytes, CardiacPatch-Clamp TechniquesPotassiumPotassium Channels, Inwardly RectifyingVentricular Function

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17394574

Citation

Bányász, T, et al. "Action Potential Clamp Fingerprints of K+ Currents in Canine Cardiomyocytes: Their Role in Ventricular Repolarization." Acta Physiologica (Oxford, England), vol. 190, no. 3, 2007, pp. 189-98.
Bányász T, Magyar J, Szentandrássy N, et al. Action potential clamp fingerprints of K+ currents in canine cardiomyocytes: their role in ventricular repolarization. Acta Physiol (Oxf). 2007;190(3):189-98.
Bányász, T., Magyar, J., Szentandrássy, N., Horváth, B., Birinyi, P., Szentmiklósi, J., & Nánási, P. P. (2007). Action potential clamp fingerprints of K+ currents in canine cardiomyocytes: their role in ventricular repolarization. Acta Physiologica (Oxford, England), 190(3), 189-98.
Bányász T, et al. Action Potential Clamp Fingerprints of K+ Currents in Canine Cardiomyocytes: Their Role in Ventricular Repolarization. Acta Physiol (Oxf). 2007;190(3):189-98. PubMed PMID: 17394574.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Action potential clamp fingerprints of K+ currents in canine cardiomyocytes: their role in ventricular repolarization. AU - Bányász,T, AU - Magyar,J, AU - Szentandrássy,N, AU - Horváth,B, AU - Birinyi,P, AU - Szentmiklósi,J, AU - Nánási,P P, Y1 - 2007/03/30/ PY - 2007/3/31/pubmed PY - 2007/12/8/medline PY - 2007/3/31/entrez SP - 189 EP - 98 JF - Acta physiologica (Oxford, England) JO - Acta Physiol (Oxf) VL - 190 IS - 3 N2 - AIM: The aim of the present study was to give a parametric description of the most important K(+) currents flowing during canine ventricular action potential. METHODS: Inward rectifier K(+) current (I(K1)), rapid delayed rectifier K(+) current (I(Kr)), and transient outward K(+) current (I(to)) were dissected under action potential clamp conditions using BaCl(2), E-4031, and 4-aminopyridine, respectively. RESULTS: The maximum amplitude of I(to) was 3.0 +/- 0.23 pA/pF and its integral was 29.7 +/- 2.5 fC/pF. The current peaked 4.4 +/- 0.7 ms after the action potential upstroke and rapidly decayed to zero with a time constant of 7.4 +/- 0.6 ms. I(Kr) gradually increased during the plateau, peaked 7 ms before the time of maximum rate of repolarization (V(max)(-)) at -54.2 +/- 1.7 mV, had peak amplitude of 0.62 +/- 0.08 pA/pF, and integral of 57.6 +/- 6.7 fC/pF. I(K1) began to rise from -22.4 +/- 0.8 mV, peaked 1 ms after the time of V(max)(-) at -58.3 +/- 0.6 mV, had peak amplitude of 1.8 +/- 0.1 pA/pF, and integral of 61.6 +/- 6.2 fC/pF. Good correlation was observed between peak I(K1) and V(max)(-) (r = 0.93) but none between I(Kr) and V(max)(-). Neither I(K1) nor I(Kr) was frequency-dependent between 0.2 and 1.66 Hz. Congruently, I(Kr) failed to accumulate in canine myocytes at fast driving rates. CONCLUSION: Terminal repolarization is dominated by I(K1), but action potential duration is influenced by several ion currents simultaneously. As I(to) was not active during the plateau, and neither I(K1) nor I(Kr) was frequency-dependent, other currents must be responsible for the frequency dependence of action potential duration at normal and slow heart rates in canine ventricular cells. SN - 1748-1708 UR - https://www.unboundmedicine.com/medline/citation/17394574/Action_potential_clamp_fingerprints_of_K+_currents_in_canine_cardiomyocytes:_their_role_in_ventricular_repolarization_ L2 - https://doi.org/10.1111/j.1748-1716.2007.01674.x DB - PRIME DP - Unbound Medicine ER -