Houchi H, Okuno M, Kitamura K, Minakuchi K, Ishimura Y, Ohuchi T, Oka M
Department of Pharmacology, School of Medicine, University of Tokushima, Japan.
Life Sci. 1995;56(21):1825-34. doi: 10.1016/0024-3205(95)00154-x.
The effect of pituitary adenylate cyclase-activating polypeptide 1-38 (PACAP1-38) on Ca2+ efflux from cultured bovine adrenal chromaffin cells was examined. PACAP1-38 stimulated the efflux of 45Ca2+ from the cells in a concentration dependent manner (10(-9)-10(-7)M). This effect was inhibited by its potent receptor antagonist PACAP6-38. PACAP1-38 increased the formation of [3H]inositol phosphates and cyclic AMP in the cells. Forskolin, an activator of adenylate cyclase, also stimulated the efflux of 45Ca2+ from the cells. 3-Isobutyl-1-methylxanthine (IBMX), an inhibitor of phosphodiesterase, enhanced PACAP1-38-induced 45Ca2+ efflux from the cells. Phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, had no effect on the efflux of 45Ca2+ from the cells. The increases in 45Ca2+ efflux induced by PACAP1-38 and forskolin were reduced by deprivation of extracellular Na+ and the Na+/Ca2+ exchange inhibitor amiloride. In addition, PACAP1-38 stimulated 22Na+ influx into the cells, and this action was inhibited by amiloride. These results suggest that PACAP1-38 stimulates an Na+/Ca2+ exchange mechanism through activation of adenylate cyclase in cultured bovine adrenal chromaffin cells.
研究了垂体腺苷酸环化酶激活多肽1 - 38（PACAP1 - 38）对培养的牛肾上腺嗜铬细胞Ca2+外流的影响。PACAP1 - 38以浓度依赖的方式（10（-9）- 10（-7）M）刺激细胞中45Ca2+的外流。其强效受体拮抗剂PACAP6 - 38可抑制这种作用。PACAP1 - 38增加了细胞中[3H]肌醇磷酸和环磷酸腺苷的形成。腺苷酸环化酶激活剂福斯高林也刺激细胞中45Ca2+的外流。磷酸二酯酶抑制剂3 - 异丁基 - 1 - 甲基黄嘌呤（IBMX）增强了PACAP1 - 38诱导的细胞中45Ca2+的外流。蛋白激酶C激活剂佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯（PMA）对细胞中45Ca2+的外流没有影响。细胞外Na+缺失和Na+/Ca2+交换抑制剂阿米洛利可减少PACAP1 - 38和福斯高林诱导的45Ca2+外流增加。此外，PACAP1 - 38刺激22Na+流入细胞，且这种作用可被阿米洛利抑制。这些结果表明，PACAP1 - 38通过激活培养的牛肾上腺嗜铬细胞中的腺苷酸环化酶来刺激Na+/Ca2+交换机制。
