Froldi G, Pandolfo L, Chinellato A, Ragazzi E, Caparrotta L, Fassina G
Department of Pharmacology, University of Padova, Italy.
Naunyn Schmiedebergs Arch Pharmacol. 1994 Apr;349(4):381-6. doi: 10.1007/BF00170884.
The effects of adenine compounds and UTP were examined in electrically driven rat left atria. ATP, ADP, AMP, adenosine and UTP caused a dual inotropic effect: first a rapid decrease in contractility, and second an increase in contractile tension. alpha,beta-Methylene ATP caused an increase in contractile tension only, whereas 2-methylthio-ATP only induced a negative inotropic effect, 1,3-Dipropyl-8-cyclopentylxanthine inhibited the negative effects of ATP and adenosine, whereas 3,7-dimethyl-1-propargylxanthine did not influence the effects of ATP. Suramin but not reactive blue 2 antagonized the positive inotropism induced by ATP and alpha,beta-methylene ATP. Suramin also abolished the positive inotropic effect induced by UTP. These results demonstrate that ATP may induce negative inotropism directly by an action on A1-adenosine receptors and positive inotropism by an action on P2x-purinoceptors. UTP induces a positive inotropic effect mediated by suramin-sensitive receptors.
在电驱动的大鼠左心房中研究了腺嘌呤化合物和UTP的作用。ATP、ADP、AMP、腺苷和UTP产生了双重变力作用：首先是收缩力迅速下降，其次是收缩张力增加。α,β-亚甲基ATP仅引起收缩张力增加，而2-甲硫基-ATP仅诱导负性变力作用，1,3-二丙基-8-环戊基黄嘌呤抑制ATP和腺苷的负性作用，而3,7-二甲基-1-丙炔基黄嘌呤不影响ATP的作用。苏拉明而非活性蓝2拮抗ATP和α,β-亚甲基ATP诱导的正性变力作用。苏拉明还消除了UTP诱导的正性变力作用。这些结果表明，ATP可能通过作用于A1-腺苷受体直接诱导负性变力作用，并通过作用于P2x嘌呤受体诱导正性变力作用。UTP诱导由苏拉明敏感受体介导的正性变力作用。
