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Trans (+-)-3,4-dichloro-N-methyl-N-[ 2-( 1-pyrrolidinyl ) cyclohexyl ]-benzeneacetamide-methanesulfonate-hydrate (U-50 488H), a specific K-agonist. at 1 - 10 μmol·L-1 caused concentration-dependent reductions in the action potential duration at 5.0% and 90% of repolarization (APD50 and APD90) without modifying the resting potential (RP), the action potential amplitude (APA) and the maximal upstroke velocity (Vmax). The effects were attenuated by (- )- (lR,5R.9R)-5,9-diethyl-2-(3-furylmethyI)-2 L - hydroxy- 6 , 7 - benzomorphan (Mr 2266 BS, 1 μmol·L-1), a specific K-antagonist which itself had no effect on the action potentials of the ventricular papillary muscle of guinea pigs, indicating that U-50 -188H at 1-10 μmol·L-1 acts via specific cardiac K-receptors. At 100 μmol·L-1, U-50 488H not only shortened APD50 and APD90 but also reduced RP, APA, and Vmax which were not attenuated by Mr 2266 BS (1 μmol·L-1) suggesting that the effects of U-50 488H at 100 μmol · L-1 were probably nonspecific.
At 1 - (4-dichloro-N-methyl-N- [2- (1-pyrrolidinyl) cyclohexyl] -benzeneacetamide-methanesulfonate- hydrate (U-50 488H) 10 μmol·L-1 caused concentration-dependent reductions in the action potential duration at 5.0% and 90% of repolarization (APD50 and APD90) without modifying the resting potential (RP), the action potential amplitude (APA) and the maximal upstroke velocity (Vmax) The effects were attenuated by (-) - (lR, 5R.9R) -5,9-diethyl- 2- 1 μmol·L-1), a specific K-antagonist which itself had no effect on the action potentials of the ventricular papillary muscle of guinea pigs, indicating that U-50 -188H at 1-10 μmol·L-1 acts via specific cardiac K-receptors. At 100 μmol·L-1, U-50 488H not only shortened APD50 and APD90 but also reduced RP, APA, and Vmax which were not attenuated by Mr 2266 BS (1 μmol·L-1) suggesting that the effects of U-50 488H at 100 μmol · L-1 were prob ably nonspecific.