血小板活化因子对豚鼠心室肌细胞动作电位和钾通道的影响.pdfVIP

282 Acta Physiologica Sinica, June 25, 2004, 56(3): 282-287 Research Paper Effects of platelet activating factor on action potentials and potassium channels in guinea-pig ventricular myocytes 1, 1,* 1 2 1 1 DU Yi-Mei , TANG Ming , LIU Chang-Jin , KE Qin-Mei , LUO Hong-Yan , HU Xin-Wu 1 Department of Physiology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China; 2Department of Geriatrics, the Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 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 µmol/L PAF increased APD90 from 225.8±23.3 to 352.8±29.8 ms (n=5, P0.05), decreased IK1 and IK tail currents from -6.1±1.3 to -5.6±1.1 nA (n=5, P0.05) 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 IK1 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 IK·ATP was activated (mimic ischemic condition), 1 µmol/L PAF shortened APD90 from 153±24.6 to 88.2±19.4 ms (n=5, P 0.01). Incubation of myocytes with 1 µmol/L glibenclamide, a blocker of IK·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 IK; while with 0 mmol/L ATP in the pipette, PAF c