Boarder M R, Marriott D, Adams M
Biochem Pharmacol. 1987 Jan 1;36(1):163-7. doi: 10.1016/0006-2952(87)90394-7.
Stimulus secretion in response to acetylcholine (or nicotine) in adrenal chromaffin cells involves calcium influx and is tetrodotoxin insensitive. The mechanism by which activation of the nicotinic acetylcholine receptor (AChR) leads to calcium influx is not clear, and the requirement for external sodium is controversial. We report that when bovine chromaffin cells are continuously perfused in the absence of sodium, secretion of catecholamines in response to 3 X 10(-5) M nicotine is not impaired. Also, secretion stimulated by this concentration of nicotine is not potently and stereospecifically inhibited by the (+)- and (-)-isomers of nicardipine. At a concentration of (+)-nicardipine (10(-7) M) which inhibits most of the release stimulated by 50 mM potassium, the response to 3 X 10(-5) M nicotine remains; however, the dose-response curve to nicotine is shifted slightly to the left. The results are discussed with respect to models of stimulus secretion coupling in bovine adrenal chromaffin cells.
肾上腺嗜铬细胞对乙酰胆碱（或尼古丁）产生的刺激分泌涉及钙内流，且对河豚毒素不敏感。烟碱型乙酰胆碱受体（AChR）激活导致钙内流的机制尚不清楚，并且外界钠的需求存在争议。我们报道，当在无钠情况下持续灌注牛嗜铬细胞时，对3×10⁻⁵ M尼古丁产生的儿茶酚胺分泌未受损害。此外，该浓度尼古丁刺激的分泌未被尼卡地平的（+）-和（-）-异构体有效且立体特异性地抑制。在抑制50 mM钾刺激的大部分释放的（+）-尼卡地平浓度（10⁻⁷ M）下，对3×10⁻⁵ M尼古丁的反应仍然存在；然而，尼古丁的剂量反应曲线略微左移。结合牛肾上腺嗜铬细胞中刺激分泌偶联模型对结果进行了讨论。
