Sorimachi M, Nishimura S, Yamagami K
Department of Physiology, Kagoshima University, School of Medicine, Japan.
Jpn J Physiol. 1994;44(4):343-56. doi: 10.2170/jjphysiol.44.343.
The concentration of cytosolic Ca2+ ([Ca]in) and catecholamine (CA) secretion were examined in bovine adrenal chromaffin cells to determine whether Ca2+ influx through nicotinic ACh receptor (nAChR) channels contributes to CA secretion induced by nAChR stimulation. Nicotine added under Na(+)-free conditions caused a marked increase in [Ca]in and quenching of fura-2 fluorescence in the presence of Mn2+, suggesting the stimulated entry of divalent cations through nAChR channels. However, nicotine-induced increase in CA secretion occurred only at a non-physiologically high external Ca2+ concentration under Na(+)-free conditions. Both the nicotine-induced increase in [Ca]in and CA secretion under Na(+)-free conditions were reduced in the presence of hexamethonium, methoxyverapamil (D600), nifedipine, Bay-K-8644, clonidine, and guanethidine. All of these agents inhibited the nicotine-induced increase in cytosolic Na+ concentration in a dose-dependent manner, as measured by SBFI microfluorometry. The present results suggest that Ca2+ influx through nAChR channels under physiological conditions may not contribute to CA secretion.
在牛肾上腺嗜铬细胞中检测了胞质Ca2+浓度（[Ca]in）和儿茶酚胺（CA）分泌，以确定通过烟碱型乙酰胆碱受体（nAChR）通道的Ca2+内流是否有助于nAChR刺激诱导的CA分泌。在无Na+条件下添加尼古丁会导致[Ca]in显著增加，并且在存在Mn2+的情况下fura-2荧光淬灭，表明二价阳离子通过nAChR通道被刺激进入。然而，尼古丁诱导的CA分泌增加仅在无Na+条件下非生理性的高细胞外Ca2+浓度时发生。在存在六甲铵、甲氧基维拉帕米（D600）、硝苯地平、Bay-K-8644、可乐定和胍乙啶的情况下，无Na+条件下尼古丁诱导的[Ca]in增加和CA分泌均减少。通过SBFI显微荧光测定法测量，所有这些药物均以剂量依赖性方式抑制尼古丁诱导的胞质Na+浓度增加。目前的结果表明，在生理条件下通过nAChR通道的Ca2+内流可能对CA分泌没有贡献。
