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Effects of platelet activating factor on action potentials and potassium channels in guinea-pig ventricular myocytes.
Sheng Li Xue Bao. 2004 Jun 25; 56(3):282-7.SL

Abstract

This study was designed to investigate the effects of platelet activating factor (PAF) on the action potential and potassium currents in guinea-pig ventricular myocytes. Whole cell patch clamp techniques were used. With 5 mmol/L ATP in the pipette electrode(mimic normal condition), 1 micromol/L PAF increased APD(90) from 225.8+/-23.3 to 352.8+/-29.8 ms (n=5, P<0.05), decreased I(K1) and I(K) tail currents from -6.1+/-1.3 to -5.6+/-1.1 nA (n=5, P<0.05) at -120 mV and from 173.5+/-16.7 to 152.1+/-11.5 pA (P<0.05, n=4) at +30 mV, respectively. But PAF had no effect on I(K1) at potentials within the normal range of membrane potentials (between -90 mV and +20 mV). In the contrary, without ATP in the pipette electrode by which I(K.ATP) was activated (mimic ischemic condition), 1 micro mol/L PAF shortened APD(90) from 153+/-24.6 to 88.2+/-19.4 ms (n=5, P<0.01). Incubation of myocytes with 1 micro mol/L glibenclamide, a blocker of I(K.ATP) could restore prolongation of APD induced by PAF. In conclusion, in guinea-pig ventricular myocytes, with 5 mmol/L ATP in the pipette PAF could prolong APD partly due to the inhibition of I(K); while with 0 mmol/L ATP in the pipette, PAF could induce an activation of I(K.ATP), hence a decrease in APD. It is suggested that PAF may amplify the heterogeneity between ischemic and normal cardiac myocytes during ischemia /reperfusion, which may play a vital role in the pathogenesis of the arrhythmias induced by ischemia /reperfusion.

Authors+Show Affiliations

Du YM
Department of Physiology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.
Tang M
No affiliation info available
Liu CJ
No affiliation info available
Ke QM
No affiliation info available
Luo HY
No affiliation info available
Hu XW
No affiliation info available

MeSH

Action PotentialsAdenosine TriphosphateAnimalsGlyburideGuinea PigsHeart VentriclesMyocytes, CardiacPatch-Clamp TechniquesPlatelet Activating FactorPotassium Channels

Pub Type(s)

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

Language

eng

PubMed ID

15224138

Citation

Du, Yi-Mei, et al. "Effects of Platelet Activating Factor On Action Potentials and Potassium Channels in Guinea-pig Ventricular Myocytes." Sheng Li Xue Bao : [Acta Physiologica Sinica], vol. 56, no. 3, 2004, pp. 282-7.
Du YM, Tang M, Liu CJ, et al. Effects of platelet activating factor on action potentials and potassium channels in guinea-pig ventricular myocytes. Sheng Li Xue Bao. 2004;56(3):282-7.
Du, Y. M., Tang, M., Liu, C. J., Ke, Q. M., Luo, H. Y., & Hu, X. W. (2004). Effects of platelet activating factor on action potentials and potassium channels in guinea-pig ventricular myocytes. Sheng Li Xue Bao : [Acta Physiologica Sinica], 56(3), 282-7.
Du YM, et al. Effects of Platelet Activating Factor On Action Potentials and Potassium Channels in Guinea-pig Ventricular Myocytes. Sheng Li Xue Bao. 2004 Jun 25;56(3):282-7. PubMed PMID: 15224138.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of platelet activating factor on action potentials and potassium channels in guinea-pig ventricular myocytes. AU - Du,Yi-Mei, AU - Tang,Ming, AU - Liu,Chang-Jin, AU - Ke,Qin-Mei, AU - Luo,Hong-Yan, AU - Hu,Xin-Wu, PY - 2004/6/30/pubmed PY - 2006/7/22/medline PY - 2004/6/30/entrez SP - 282 EP - 7 JF - Sheng li xue bao : [Acta physiologica Sinica] JO - Sheng Li Xue Bao VL - 56 IS - 3 N2 - This study was designed to investigate the effects of platelet activating factor (PAF) on the action potential and potassium currents in guinea-pig ventricular myocytes. Whole cell patch clamp techniques were used. With 5 mmol/L ATP in the pipette electrode(mimic normal condition), 1 micromol/L PAF increased APD(90) from 225.8+/-23.3 to 352.8+/-29.8 ms (n=5, P<0.05), decreased I(K1) and I(K) tail currents from -6.1+/-1.3 to -5.6+/-1.1 nA (n=5, P<0.05) at -120 mV and from 173.5+/-16.7 to 152.1+/-11.5 pA (P<0.05, n=4) at +30 mV, respectively. But PAF had no effect on I(K1) at potentials within the normal range of membrane potentials (between -90 mV and +20 mV). In the contrary, without ATP in the pipette electrode by which I(K.ATP) was activated (mimic ischemic condition), 1 micro mol/L PAF shortened APD(90) from 153+/-24.6 to 88.2+/-19.4 ms (n=5, P<0.01). Incubation of myocytes with 1 micro mol/L glibenclamide, a blocker of I(K.ATP) could restore prolongation of APD induced by PAF. In conclusion, in guinea-pig ventricular myocytes, with 5 mmol/L ATP in the pipette PAF could prolong APD partly due to the inhibition of I(K); while with 0 mmol/L ATP in the pipette, PAF could induce an activation of I(K.ATP), hence a decrease in APD. It is suggested that PAF may amplify the heterogeneity between ischemic and normal cardiac myocytes during ischemia /reperfusion, which may play a vital role in the pathogenesis of the arrhythmias induced by ischemia /reperfusion. SN - 0371-0874 UR - https://www.unboundmedicine.com/medline/citation/15224138/Effects_of_platelet_activating_factor_on_action_potentials_and_potassium_channels_in_guinea_pig_ventricular_myocytes_ DB - PRIME DP - Unbound Medicine ER -