Nakazawa K, Saito H, Matsuki N
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 1992 Nov;346(5):515-22. doi: 10.1007/BF00169006.
Effects of calcitonin gene-related peptide (CGRP), a putative non-adrenergic non-cholinergic neutrotransmitter on the electrical properties of the cell membrane, were investigated in enzymically dispersed smooth muscle cells from rat vas deferens. Under current clamp conditions, CGRP (up to 10(-7) M) did not induce significant changes in membrane potentials or input resistance in the resting state. The configurations of action potentials elicited by depolarizing current pulses were also unaffected, except that a prolongation of the duration of the action potentials by a high dose (10(-7) M) of CGRP was observed in some of the cells. Under whole cell voltage clamp conditions, the transient and sustained K+ currents, activated by depolarizing voltage-steps, were apparently decreased in the presence of 10(-9) to 10(-7) M CGRP. The peptide increased the voltage-gated Ca2+ current in cells loaded with 145 mM Cs+ solution in order to block the K+ currents. The voltage-dependency of the peak Ca2+ current was not changed by CGRP. Ba2+ (10.8 mM) was used as a charge carrier for the Ca(2+)-channel current to clarify further the effects of CGRP on the properties of the current. CGRP (10(-8) M) delayed the inactivation time course of the Ca(2+)-channel current and slowed the recovery from inactivation. The peptide did not affect the steady-state inactivation measured by changing the holding potential. The Ca(2+)-channel current in the presence of CGRP was suppressed by nicardipine (10(-6) M) to the same extent as the current under control conditions. The results suggest that CGRP modifies the L-type Ca2+ channel in smooth muscle cells.
在大鼠输精管酶分散的平滑肌细胞中,研究了降钙素基因相关肽(CGRP),一种假定的非肾上腺素能非胆碱能神经递质,对细胞膜电特性的影响。在电流钳制条件下,CGRP(高达10⁻⁷ M)在静息状态下未引起膜电位或输入电阻的显著变化。除了在一些细胞中观察到高剂量(10⁻⁷ M)的CGRP使动作电位持续时间延长外,去极化电流脉冲引发的动作电位形态也未受影响。在全细胞电压钳制条件下,去极化电压阶跃激活的瞬时和持续K⁺电流在存在10⁻⁹至10⁻⁷ M CGRP时明显降低。该肽增加了用145 mM Cs⁺溶液加载以阻断K⁺电流的细胞中的电压门控Ca²⁺电流。CGRP未改变峰值Ca²⁺电流的电压依赖性。使用Ba²⁺(10.8 mM)作为Ca²⁺通道电流的电荷载体,以进一步阐明CGRP对电流特性的影响。CGRP(10⁻⁸ M)延迟了Ca²⁺通道电流的失活时间进程,并减缓了失活后的恢复。该肽不影响通过改变钳制电位测量的稳态失活。尼卡地平(10⁻⁶ M)在CGRP存在下对Ca²⁺通道电流的抑制程度与对照条件下的电流相同。结果表明,CGRP修饰了平滑肌细胞中的L型Ca²⁺通道。