Liu P S, Lin M K, Hsieh H L
Department of Microbiology, Soochow University, Shihlin, Taipei, Taiwan.
Neurosci Lett. 1996 Feb 9;204(3):181-4. doi: 10.1016/0304-3940(96)12350-8.
Dehydroepiandrosterone sulfate (DHEAS) dose-dependently inhibited [3H]norepinephrine (NE) secretion and the corresponding [Ca2+]i rise induced by the nicotinic receptor agonist 1,1-dimethyl-4-phenylpoperazimium (DMPP) in bovine chromaffin cells. DHEAS at 10 microM, the physiological concentration in human serum, significantly inhibited both the release of [3H]NE and the rise of [Ca2+]i induced by DMPP in chromaffin cells. DHEAS also inhibited the [3H]NE release induced by the Na+ channel activator veratridine. However, DHEAS did not affect either the [3H]NE release, or the corresponding [Ca2+]i rise induced by high K+. Moreover, DHEAS suppressed the [Na+]i rise induced by either DMPP or high K+ as monitored by the fluorescence 340/380 ratio of SBFI loaded chromaffin cells. Our results suggest that the inhibitory effects of DHEAS on secretion mainly occur at nicotinic receptors as well as at the voltage-dependent Na+ channels.
硫酸脱氢表雄酮（DHEAS）呈剂量依赖性地抑制牛嗜铬细胞中烟碱样受体激动剂1,1 - 二甲基 - 4 - 苯基哌嗪（DMPP）诱导的[3H]去甲肾上腺素（NE）分泌以及相应的细胞内钙离子浓度（[Ca2+]i）升高。在人血清中的生理浓度10微摩尔/升时，DHEAS显著抑制嗜铬细胞中DMPP诱导的[3H]NE释放和[Ca2+]i升高。DHEAS还抑制了钠离子通道激活剂藜芦碱诱导的[3H]NE释放。然而，DHEAS对高钾诱导的[3H]NE释放或相应的[Ca2+]i升高均无影响。此外，通过监测装载了SBFI的嗜铬细胞的荧光340/380比值发现，DHEAS抑制了DMPP或高钾诱导的细胞内钠离子浓度（[Na+]i）升高。我们的结果表明，DHEAS对分泌的抑制作用主要发生在烟碱样受体以及电压依赖性钠离子通道上。
