|摘要：||Dapagliﬂozin(DAPA)orcanagliﬂozin(CANA),Na+-dependentglucoseco-transportertype 2(SGLT2) inhibitors, were used for treatment of type II diabetes mellitus. Addition of DAPA or CANA suppressed M-type K+ current (IK(M))inpituitarytumor(GH3)andpheochromocytomaPC12cells.TheIC50 valueforDAPA-orCANA-mediated inhibition of IK(M) in GH3 cells was 0.11 or 0.42 μM, respectively. The presence of DAPA (0.1 μM) shifted the steady-state activation of IK(M) to less depolarized potential without changing the gating charge of the current. During high-frequency depolarizing pulses, IK(M) magnitude was reduced by DAPA; however, DAPA-induced block of IK(M) remained eﬀective. The amplitude of neither erg-mediated K+ current nor hyperpolarizationactivated cation current in GH3 cells was modiﬁed in the presence of 1 μM DAPA. Alternatively, addition of DAPA, CANA, phlorizin or chlorotoxin eﬀectively suppressed α-methylglucoside-(αMG-) induced current (IαMG) in GH3 cells, albeit inability of teﬂuthrin (activator of INa) to suppress this current. DAPA shifted the chargevoltage relation of presteady-state IαMG in a rightward and downward direction with no change in the gating charge of the IαMG. Under current-clamp recordings, subsequent additions of DAPA, but still in the continued presence of αMG, increased the ﬁring rate of spontaneous action potentials stimulated by αMG. Our results suggested that activity of SGLT was expressed functionally in GH3 and PC12 cells. Therefore, inhibitory actions of DAPA or CANA on the amplitude and gating of IK(M) might provide a yet unidentiﬁed mechanism through which the SGLT1 or SGLT2 activity were attenuated in unclamped cells occurring in vivo.