Uchiyama Y, Morita K, Kitayama S, Suemitsu T, Minami N, Miyasako T, Dohi T
Department of Pharmacology, Hiroshima University School of Dentistry, Japan.
Jpn J Pharmacol. 1994 May;65(1):73-7. doi: 10.1254/jjp.65.73.
The role of nitric oxide (NO) in neurotransmitter release was studied using bovine adrenal medullary chromaffin cells. L-Arginine and sodium nitroprusside (SNP) slightly increased the intracellular free calcium concentration ([Ca2+]i), and the effects of the agents were dependent on the presence of the extracellular Ca2+ ([Ca2+]o), but were not blocked by verapamil (30 microM) or diltiazem (30 microM). SNP enhanced the acetylcholine (ACh)-induced rise in [Ca2+]i in the presence but not in the absence of [Ca2+]o. The effects of L-arginine but not those of SNP were inhibited by N omega-nitro-L-arginine (L-NNA). L-NNA significantly reduced the ACh-induced rise in [Ca2+]i and catecholamine (CA) release, and the reduction was restored by L-arginine but not by D-arginine. These results suggest a possible involvement of NO in ACh-induced [Ca2+]i rise and CA release in bovine adrenal chromaffin cells.
利用牛肾上腺髓质嗜铬细胞研究了一氧化氮（NO）在神经递质释放中的作用。L-精氨酸和硝普钠（SNP）可轻微增加细胞内游离钙浓度（[Ca2+]i），且这些药物的作用依赖于细胞外钙（[Ca2+]o）的存在，但不受维拉帕米（30微摩尔）或地尔硫䓬（30微摩尔）的阻断。在有[Ca2+]o存在时，SNP可增强乙酰胆碱（ACh）诱导的[Ca2+]i升高，但在无[Ca2+]o时则无此作用。Nω-硝基-L-精氨酸（L-NNA）可抑制L-精氨酸的作用，但不抑制SNP的作用。L-NNA可显著降低ACh诱导的[Ca2+]i升高和儿茶酚胺（CA）释放，L-精氨酸可恢复这种降低，但D-精氨酸则不能。这些结果提示，NO可能参与牛肾上腺嗜铬细胞中ACh诱导的[Ca2+]i升高和CA释放。
