Aloj S M, Liguoro D, Kiang J G, Smallridge R C
Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
Biochem Biophys Res Commun. 1993 Aug 31;195(1):1-7. doi: 10.1006/bbrc.1993.2000.
In the epithelial cell line FRT, derived from rat thyroid, extracellular ATP, at a concentration as low as 1 x 10(-7) M, specifically increases cytosolic Ca++ two fold over the basal level of 255 +/- 45 nM. A maximum increase of 5 fold over basal is seen at 1 x 10(-5) M ATP. The effect occurs in the absence of any measurable phosphatidyl inositol metabolism and requires the presence of extracellular Ca++, but is independent of extracellular Na+; it is duplicated by ATP gamma S but not by adenosine, AMP, ADP, AMP-PNP, AMP-CPP, or AMP-PCP. In the presence of the P2-receptor antagonist suramin, the ATP induced Ca++ influx is completely inhibited, whereas Mg++, La , and verapamil are ineffective. It appears that the most likely (and unique) mechanism of ATP induced increase of cytosolic Ca++ in FRT cells in an increased influx through the activation of a P2 receptor operated Ca++ channel.
在源自大鼠甲状腺的上皮细胞系FRT中，细胞外ATP浓度低至1×10⁻⁷ M时，可使胞质Ca²⁺浓度比基础水平255±45 nM增加两倍。在1×10⁻⁵ M ATP时，可观察到比基础水平最多增加五倍。该效应在没有任何可测量的磷脂酰肌醇代谢的情况下发生，并且需要细胞外Ca²⁺的存在，但与细胞外Na⁺无关；ATPγS可复制该效应，但腺苷、AMP、ADP、AMP-PNP、AMP-CPP或AMP-PCP则不能。在P2受体拮抗剂苏拉明存在的情况下，ATP诱导的Ca²⁺内流被完全抑制，而Mg²⁺、La³⁺和维拉帕米则无效。看来，ATP诱导FRT细胞胞质Ca²⁺增加的最可能（也是独特）机制是通过激活P2受体操纵的Ca²⁺通道使内流增加。
