Purification and characterization of glutathione reductase from Scots pine needles

Changes in the excitability of the liverwort Conocephalum conicum L. caused by inhibitors of ionic channels and phosphorylation uncouplers, were examined. Action potentials were triggered by electrical and light stimuli. Tetraethylammonium chloride, an inhibitor of K⁺ channels, completely blocked the ability to generate action potentials. Excitability also disappeared under the influence of MnCl₂ and LaCl₃, inhibitors of Ca²⁺ channels. The participation of Ca²⁺ and K⁺ in the electrogenesis of action potentials in C. conicum is discussed. Treatment with phosphorylation uncouplers induced a gradual disappearance of the metabolic component of the resting potential. It was accompanied by some series of excitations, numbering from several to over a dozen impulses characterized by decreasing amplitudes, after which the organism became totally unexcitable. Dicyclohexylcarbodiimide an inhibitor of H⁺-ATPase, also caused depolarization of the transmembrane potential and disappearance of excitability. The results indicated the participation of a metabolic component in the generation of action potentials in C. conicum .     

A dual action of taurine on the delayed rectifier K+ current in embryonic chick cardiomyocytes

Summary Effects of taurine on the delayed rectifier K⁺ channel in isolated 10-day-old embryonic chick ventricular cardiomyocytes were examined at different intracellular Ca²⁺ concentrations ([Ca]_i), using whole-cell voltage and current clamp techniques. Experiments were performed at room temperature (22°C). Test pulses were applied between -20 to +90m V from a holding potential of -40mV. When [Ca]_i was pCa 7, addition of 10 and 20 mM taurine to the bath solution reduced the delayed rectifier K⁺ current (I_K) at +90mV by 17.4 ± 2.8% (n = 5, P < 0.01) and 25.5 ± 2.6% (n = 5, P < 0.001), respectively. In contrast, when [Ca]_i was pCa 10, I_K at +90 mV was enhanced by 19.1 ± 3.1% (n = 7, P < 0.01) at 10mM taurine, and by 29.3 ± 2.4% (n = 7, P < 0.001) at 20mM taurine. The voltage of half-maximum activation (V_1/2) was shifted in a hyperpolarizing direction; at pCa 7, the value was +0.2 ± 2.2mV (n = 5) in control and -10.6 ± 1.8mV (n = 5) in 20mM taurine. At pCa 10, the V_1/2 value was +18.5 ± 4.6mV (n = 5) in control and +6.6 ± 5.2mV (n = 5) in taurine (20mM). Taurine decreased the action potential duration (APD) at pCa 10, but at pCa 7 did not affect it. In addition, taurine enhanced the transient outward current in a concentration-dependent manner. These results indicate that taurine modulates the delayed rectifier K⁺ channel, an effect dependent on [Ca]_i and capable of regulating APD.