Abstract: Aim To observe the effects of protein kinase A (PKA), protein kinase C(PKC)inhibitorand dephosphory lating agent on ATP-sensitive potassium current($I_{KATP}$)of rat ventricularcardiomy ocytes andinvestiga te the mechanismof cromakalim opening $I_{KATP}$.Methods Whole-cell patch-clamp was used torecord $I_{KATP}$.Results Cromakalim (1 μmol·L^-1)was shown to induce $I_{KATP}$ at the holding potential of 10 mV, 37 ℃.When added to the pipet tesolution, the PKA inhibitor PKI(6 ~ 22)amide (1 μmol·L^-1)caused production of $I_{KATP}$, just as cromakalim did, whilethe PKC inhibitor calphostic C(1 μmol·L^-1)showed no Effect.Moreover, addition of the dephosphory lating agent, butanedione monoxime(5 mmol·L^-1), to the bath also stimulated $I_{KATP}$.Conclusion The mechanismof cromakalim opening $I_{KATP}$ is due to the inhibition of PKA (not PKC).

Key words: cromakalim, ATP-sensitirepotassium current($I_{KATP}$), protein kinase A, protein kinase C