Fig. 5. LPI elicits a biphasic change in membrane potential in RBMVEC.

A, Averaged changes in membrane potential ± SEM. in response to LPI (10 μM) in the absence or presence of the GPR55 antagonist, ML-193 (10 μM), or of inhibitors of small- and intermediate-conductance Ca²⁺-activated K⁺ channels (K_Ca), apamin (1 μM), and charibdotoxin (100 nM). Treatment of RBMVEC with LPI (10 μM) induced a fast and transient depolarization followed by a long-lasting hyperpolarization. The response to LPI was prevented by ML-193; the hyperpolarization phase was sensitive to apamin and charibdotoxin. B, Comparison of the average amplitude ± SEM of the hyperpolarization produced by LPI in the absence and presence of ML-193 and of apamin and charibdotoxin. (*P < 0.05; NS – not significant).