Effects of the antiarrhythmic agent tedisamil on cardiac potassium currents in humans (part 4). RESULTS

21 Aug

Action potentials of human atrial myocytes are much shorter in duration and possess a less prominent plateau than those in subepicardial ventricular myocytes (Figure 1).The current measured with this slow ramp should not be contaminated significantly by rapidly activating and inactivating currents such as sodium and calcium currents, although window currents contribute if present. IK1 was much smaller in atrial than in ventricular myocytes. At -100 mV, mean current density was -1.1±0.1 pA/pF in atrial myocytes (n=50) and -2.8±0.4 pA/pF in ventricular myocytes (n=18). In addition, outward currents positive to -20 mV were significantly larger in atrial cells, which suggests that a substantial noninactivating outward current contributes to repolarization during the plateau phase of atrial myocytes. Although almokalant, E-4031 and te-disamil clearly prolonged the action potential duration of human papillary muscle , no delayed rectifier Ik could be detected in either atrial or subepicardial ventricular myocytes.

Effects of the antiarrhythmic agent tedisamil on cardiac potassium currents in humans

Figure 1 A,B Action potentials (stimulation rate 0.5 Hz; room temperature). C,D Current voltage relations of the inward rectifier potassium current in human atrial and subepicardial ventricular myocytes (digitized data from currents activated by voltage ramps from -100 mV to +40 mV, duration 16 s [holding potential -80 mV, inset in D]). Currents are expressed as current densities (pA/pF); values are mean ± SEM from 50 atrial and 18 ventricular myocytes. Im Membrane current; Vm Membrane voltage
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