Kurosaki F
Cell Biology Laboratory, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Sugitani, Japan.
FEBS Lett. 1997 May 12;408(1):115-9. doi: 10.1016/s0014-5793(97)00403-1.
Treatment of cultured carrot cells with dibutyryl cAMP or forskolin resulted in the appreciable decrease in extracellular K+ concentration. This decrease was found to be transient and the concentration of the ion in the culture medium restored to the original level within few minutes. The cAMP-induced decrease in K+ level in the medium was almost completely inhibited when carrot cells were incubated in the presence of K+ channel blockers, CsCl and tetraethylammonium chloride. Appreciable amounts of 45Ca2+ were discharged from 45Ca2+-loaded inside-out vesicles of carrot plasma membrane by the stimulation with cAMP, however, the release of the ion was significantly inhibited in the presence of the K+ channel blockers. The release of 45Ca2+ from the vesicles was also observed when K+ current was evoked with an ionophore, valinomycin, even in the absence of cAMP. These results suggest that the gating of some of the inward K+ channels located at plasma membrane of cultured carrot cells is controlled by cytoplasmic concentration of cAMP and the inward K+ current across the plasma membrane induced by the nucleotide elicits Ca2+ influx into the cells possibly by the activation of voltage-dependent Ca2+ channels.
用二丁酰环磷腺苷(dibutyryl cAMP)或福斯可林(forskolin)处理培养的胡萝卜细胞,导致细胞外钾离子(K⁺)浓度显著降低。发现这种降低是短暂的,培养基中离子的浓度在几分钟内恢复到原始水平。当胡萝卜细胞在钾离子通道阻滞剂氯化铯(CsCl)和四乙铵氯化物存在的情况下孵育时,环磷腺苷诱导的培养基中钾离子水平的降低几乎被完全抑制。通过环磷腺苷刺激,相当数量的⁴⁵Ca²⁺从负载有⁴⁵Ca²⁺的胡萝卜质膜内翻囊泡中释放出来,然而,在钾离子通道阻滞剂存在的情况下,离子的释放被显著抑制。当用离子载体缬氨霉素(valinomycin)诱发钾离子电流时,即使在没有环磷腺苷的情况下,也观察到囊泡中⁴⁵Ca²⁺的释放。这些结果表明,培养的胡萝卜细胞质膜上一些内向钾离子通道的门控受细胞质中环磷腺苷浓度的控制,并且由该核苷酸诱导的跨质膜的内向钾离子电流可能通过激活电压依赖性钙离子通道引起钙离子流入细胞。