Simmons N L
Br J Pharmacol. 1981 Jun;73(2):379-84. doi: 10.1111/j.1476-5381.1981.tb10432.x.
1 Exogenous adenosine triphosphate (ATP) stimulates the short circuit current (SCC) in a cultured renal-derived epithelium (MDCK). Half-maximal stimulation is achieved at 1.91 X 10(-5) M ATP. 2 It is suggested that ATP interacts with a P2 purine receptor upon the basis of (a) agonist potency (ATP greater than adenosine diphosphate much greater than adenosine monophosphate, adenosine; ATP greater than uridine triphosphate greater than inosine triphosphate much greater than cytosine triphosphate, guanosine triphosphate); (b) the inhibition of the ATP response by quinidine (1 X 10(-3) M) but not by theophylline (1 X 10(-3) M). 3 Indomethacin (1 X 10(-5) M) inhibits the response of the cultured epithelium to ATP. 4 Prostaglandin E1 (PGE1) stimulates SCC but potentiates the effect of ATP on SCC. The divalent cationic ionophore A23187 (1 X 10(-6) M) transiently stimulates SCC itself and abolishes ATP-induced stimulation of the SCC.
外源性三磷酸腺苷(ATP)可刺激培养的肾源性上皮细胞(MDCK)中的短路电流(SCC)。在1.91×10⁻⁵ M ATP时可达到最大刺激效应的一半。
基于以下几点表明ATP与P2嘌呤受体相互作用:(a)激动剂效力(ATP>二磷酸腺苷>>一磷酸腺苷、腺苷;ATP>三磷酸尿苷>三磷酸肌苷>>三磷酸胞苷、三磷酸鸟苷);(b)奎尼丁(1×10⁻³ M)可抑制ATP反应,而茶碱(1×10⁻³ M)则不能。
吲哚美辛(1×10⁻⁵ M)可抑制培养的上皮细胞对ATP的反应。
前列腺素E1(PGE1)可刺激SCC,但可增强ATP对SCC的作用。二价阳离子载体A23187(1×10⁻⁶ M)可短暂刺激SCC本身,并消除ATP诱导的SCC刺激。