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Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress.
Acta Pharmacol Sin. 2004 Jun; 25(6):751-5.AP

Abstract

AIM

To determine the changes of delayed rectifier K(+) currents (I(k)) and inward rectifier K(+) currents (I(k1)) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment.

METHODS

H(2)O(2) 50 micromol/L (24 h) was used for inducing apoptosis in the cardiomyocytes culture of neonatal rats and to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by TUNEL methods and voltage-dependent K(+) currents were recorded by patch-clamp techniques.

RESULTS

H(2)O(2) 50 micromol/L (24 h) induced cell apoptosis in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K(+) currents densities (I(k), I(k1)) were down-regulated. The densities of the delayed rectifier K(+) currents (I(k)) in 50 micromol/L H(2)O(2) group were 2.52+/-0.57 pA/pF vs 5.73+/-1.84 pA/pF in the control group at +50 mV (n=8, P<0.01). The densities of the inward rectifier K(+) currents (I(k1)) in 50 micromol/L H(2)O(2) group were -13.9+/-2.70 pA/pF, 2.52+/-0.57 pA/pF vs -59.7+/-11.9 pA/pF, 5.73+/-1.84 pA/pF in the control group at -120 mV (n=8, P<0.01) and -40 mV (n=8, P<0.05), respectively. The extent of inward rectifier property of I(k1) was weakened by 50 micromol/L H(2)O(2) treatment.

CONCLUSION

The densities of I(k), I(k1) in the cardiomyocytes of guinea pigs were down-regulated and the inward rectifier property of I(k1) was weakened during the gradual apoptotic process after 50 micromol/L H(2)O(2) treatment for 24 h.

Authors+Show Affiliations

Dong DL
Department of pharmacology, Harbin Medical University, Harbin 150086, China.
Liu Y
No affiliation info available
Zhou YH
No affiliation info available
Song WH
No affiliation info available
Wang H
No affiliation info available
Yang BF
No affiliation info available

MeSH

AnimalsAnimals, NewbornApoptosisCells, CulturedDown-RegulationGuinea PigsHeart VentriclesHydrogen PeroxideMyocytes, CardiacOxidative StressPatch-Clamp TechniquesPotassium ChannelsPotassium Channels, Inwardly RectifyingRatsRats, Wistar

Pub Type(s)

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

Language

eng

PubMed ID

15169627

Citation

Dong, De-Li, et al. "Decreases of Voltage-dependent K+ Currents Densities in Ventricular Myocytes of Guinea Pigs By Chronic Oxidant Stress." Acta Pharmacologica Sinica, vol. 25, no. 6, 2004, pp. 751-5.
Dong DL, Liu Y, Zhou YH, et al. Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress. Acta Pharmacol Sin. 2004;25(6):751-5.
Dong, D. L., Liu, Y., Zhou, Y. H., Song, W. H., Wang, H., & Yang, B. F. (2004). Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress. Acta Pharmacologica Sinica, 25(6), 751-5.
Dong DL, et al. Decreases of Voltage-dependent K+ Currents Densities in Ventricular Myocytes of Guinea Pigs By Chronic Oxidant Stress. Acta Pharmacol Sin. 2004;25(6):751-5. PubMed PMID: 15169627.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress. AU - Dong,De-Li, AU - Liu,Yan, AU - Zhou,Yu-Hong, AU - Song,Wei-Hua, AU - Wang,He, AU - Yang,Bao-Feng, PY - 2004/6/1/pubmed PY - 2004/8/11/medline PY - 2004/6/1/entrez SP - 751 EP - 5 JF - Acta pharmacologica Sinica JO - Acta Pharmacol Sin VL - 25 IS - 6 N2 - AIM: To determine the changes of delayed rectifier K(+) currents (I(k)) and inward rectifier K(+) currents (I(k1)) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment. METHODS: H(2)O(2) 50 micromol/L (24 h) was used for inducing apoptosis in the cardiomyocytes culture of neonatal rats and to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by TUNEL methods and voltage-dependent K(+) currents were recorded by patch-clamp techniques. RESULTS: H(2)O(2) 50 micromol/L (24 h) induced cell apoptosis in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K(+) currents densities (I(k), I(k1)) were down-regulated. The densities of the delayed rectifier K(+) currents (I(k)) in 50 micromol/L H(2)O(2) group were 2.52+/-0.57 pA/pF vs 5.73+/-1.84 pA/pF in the control group at +50 mV (n=8, P<0.01). The densities of the inward rectifier K(+) currents (I(k1)) in 50 micromol/L H(2)O(2) group were -13.9+/-2.70 pA/pF, 2.52+/-0.57 pA/pF vs -59.7+/-11.9 pA/pF, 5.73+/-1.84 pA/pF in the control group at -120 mV (n=8, P<0.01) and -40 mV (n=8, P<0.05), respectively. The extent of inward rectifier property of I(k1) was weakened by 50 micromol/L H(2)O(2) treatment. CONCLUSION: The densities of I(k), I(k1) in the cardiomyocytes of guinea pigs were down-regulated and the inward rectifier property of I(k1) was weakened during the gradual apoptotic process after 50 micromol/L H(2)O(2) treatment for 24 h. SN - 1671-4083 UR - https://www.unboundmedicine.com/medline/citation/15169627/Decreases_of_voltage_dependent_K+_currents_densities_in_ventricular_myocytes_of_guinea_pigs_by_chronic_oxidant_stress_ DB - PRIME DP - Unbound Medicine ER -