Zhang G H, Melvin J E
Department of Dental Research, University of Rochester, NY 14642.
FEBS Lett. 1993 Jul 19;327(1):1-6. doi: 10.1016/0014-5793(93)81026-v.
The effects of inhibitors of the intracellular Ca2+ release mechanism on divalent cation fluxes were examined in acinar cells loaded with the Ca(2+)-sensitive, Mn(2+)-quenchable dye, fura-2. TMB-8 and dantrolene (DTL) dramatically inhibited the carbachol (CCh)-stimulated increase in [Ca2+]i and Mn2+ influx. These agents do not directly inhibit divalent cation entry since addition of TMB-8 or DTL after CCh stimulation did not block Mn2+ influx. TMB-8 did not influence the [Ca2+]i increase or the Mn2+ influx produced by thapsigargin. These results indicate that TMB-8 and DTL do not interfere with divalent cation influx by inhibiting a step distal to depletion of the intracellular Ca2+ pool. TMB-8 and DTL did not significantly influence the muscarinic-stimulated production of inositol trisphosphate (IP3) and inositol tetrakisphosphate (IP4), although TMB-8, but not DTL, did decrease the CCh-stimulated 1,4,5-IP3 levels approximately 55%. The above results directly demonstrate that the filling state of the intracellular Ca2+ store primarily regulates the Ca2+ entry mechanism in sublingual mucous acinar cells.
在加载了对Ca(2+)敏感、可被Mn(2+)淬灭的染料fura-2的腺泡细胞中,研究了细胞内Ca2+释放机制抑制剂对二价阳离子通量的影响。TMB-8和丹曲林(DTL)显著抑制了卡巴胆碱(CCh)刺激引起的[Ca2+]i升高和Mn2+内流。这些药物并不直接抑制二价阳离子的进入,因为在CCh刺激后添加TMB-8或DTL并没有阻断Mn2+内流。TMB-8不影响毒胡萝卜素引起的[Ca2+]i升高或Mn2+内流。这些结果表明,TMB-8和DTL不会通过抑制细胞内Ca2+池耗竭远端的步骤来干扰二价阳离子内流。TMB-8和DTL对毒蕈碱刺激产生的肌醇三磷酸(IP3)和肌醇四磷酸(IP4)没有显著影响,尽管TMB-8(而非DTL)确实使CCh刺激的1,4,5-IP3水平降低了约55%。上述结果直接表明,细胞内Ca2+储存的充盈状态主要调节舌下粘液腺泡细胞中的Ca2+进入机制。