Bott A, Eltze M, Illes P
Department of Pharmacology, Byk Gulden Pharmaceuticals, Konstanz, Germany.
Eur J Pharmacol. 1992 Mar 17;213(1):141-4. doi: 10.1016/0014-2999(92)90244-x.
Right ventricular papillary muscles of the guinea-pig heart were electrically stimulated. Cromakalim 10-100 microM and Ro 31-6930 3 microM depressed the contractile force and shortened the duration of action potentials. Glibenclamide 0.3-3 microM, ATP 100 microM and alpha, beta-methylene ATP (alpha, beta-meATP) 30 microM antagonized these effects. Suramin 300 microM failed to reverse the alpha, beta-meATP-evoked antagonism of the action of cromakalim. It is concluded that both intra- and extracellular ATP may interfere with potassium channel openers and that extracellular ATP does not act via the known P2-purinoceptor subtypes.
对豚鼠心脏的右心室乳头肌进行电刺激。10 - 100微摩尔的克罗卡林和3微摩尔的Ro 31 - 6930可降低收缩力并缩短动作电位时程。0.3 - 3微摩尔的格列本脲、100微摩尔的ATP和30微摩尔的α,β - 亚甲基ATP（α,β - meATP）可拮抗这些作用。300微摩尔的苏拉明未能逆转α,β - meATP引起的对克罗卡林作用的拮抗。结论是细胞内和细胞外的ATP均可干扰钾通道开放剂，且细胞外ATP并非通过已知的P2 - 嘌呤受体亚型发挥作用。
