FIGURE 5.
The PP1/PP2A inhibitor cantharidin inhibits the delayed recovery of ICl(Ca) in pulmonary arterial myocytes dialyzed with no ATP. A, graph showing the impact of the internal application of 100 nm cantharidin, a compound displaying higher selectivity for inhibiting PP2A over PP1, on the mean time course of normalized late ICl(Ca) at +90 mV (1-s steps at 10-s intervals) in cells lacking a supply of exogenous ATP. Cantharidin (empty squares; n = 12) enhanced the initial rundown of ICl(Ca) and prevented the delayed recovery seen under control conditions (filled squares; n = 9). ***, significantly different from control (no cantharidin) with p < 0.001. B, graph showing the mean current-voltage relationships obtained in the presence (empty squares; n = 12) or absence (filled squares; n = 9) of 100 nm cantharidin. The inhibitor successfully blocked the outwardly rectifying current by ∼58 and 64% at +20 and +130 mV, respectively. At +130 mV, the population means are significantly different with p < 0.001 (***). Both control- and cantharidin-treated cells reversed near ECl.