Glitsch H G, Rasch R
Pflugers Arch. 1986 Feb;406(2):144-50. doi: 10.1007/BF00586675.
Noradrenaline (NA; 10(-9) to 10(-6) M) depolarizes the cell membrane of quiescent sheep Purkinje fibres at resting potential level. A corresponding inward shift of the holding current occurs in voltage clamped preparations in a potential range between ca. -40 and -100 mV. The depolarizing effect is present in phentolamine (1.5 X 10(-6) M) containing solution, mimicked by isoprenaline, blocked by propranolol (5 X 10(-6) M) and is therefore supposed to be beta-adrenoceptor mediated. The inward shift of the holding current is half maximum at 60 nM noradrenaline. The shift is accompanied with an increase of the intracellular Na activity (aiNa) of the fibres as measured by Na sensitive microelectrodes. Both, the inward shift of the holding current and the accompanying aiNa increased are strongly inhibited by 2 mM CsCl. It is concluded that the depolarizing action of noradrenaline is mainly caused by the known catecholamine induced shift of the steady state activation curve of the pacemaker current (if). The shift increases if in a potential range between -40 and -100 mV and augments thereby aiNa.
去甲肾上腺素(NA;10⁻⁹至10⁻⁶M)在静息电位水平使静止的绵羊浦肯野纤维细胞膜去极化。在电压钳制标本中,在约 -40至 -100 mV的电位范围内,钳制电流会相应地向内偏移。在含有酚妥拉明(1.5×10⁻⁶M)的溶液中仍存在去极化作用,异丙肾上腺素可模拟该作用,普萘洛尔(5×10⁻⁶M)可阻断该作用,因此推测其为β - 肾上腺素能受体介导。钳制电流向内偏移在去甲肾上腺素浓度为60 nM时达到最大值的一半。该偏移伴随着用钠敏感微电极测量的纤维细胞内钠活性(aiNa)的增加。钳制电流的向内偏移以及伴随的aiNa增加均受到2 mM CsCl的强烈抑制。得出的结论是,去甲肾上腺素的去极化作用主要是由已知的儿茶酚胺诱导的起搏电流(if)稳态激活曲线的偏移引起的。这种偏移在 -40至 -100 mV的电位范围内增加if,从而增加aiNa。