Figure 4: Effect of exchange protein directly activated by cAMP inhibitor and N-butanol on AE. After 160 min of incubation (Control), 0.5% butanol (N-butanol) or 10 μmol l−1 EPAC specific inhibitor 09 (ESI09) were added. The AE inducers are: 8-(4-Chlorophenylthio)-2'-O-methyladenosine-3′,5′-cyclic (8pCPT; 0.1 μmol l−1), N-[2-(p-bromocinnamylamino)ethyl]-5isoquinolinesulfonamide (H89; 50 μmol l−1), TG (3 μmol l−1), angiotensin II (Ang II; 10 nmol l−1), polyphosphoinositide-binding-peptide (PBP10; 1 μmol l−1), 8-(4-Chlorophenylthio)adenosine 3′,5′-cyclic (8pCPT**; 50 μmol l−1) and antibiotic A23187 calcium ionophore (A23187; 10 μmol l−1). The values represent the mean ± standard deviation of duplicates from three experiments from three different donors.*P < 0.05, **P < 0.01, and***P < 0.001, significant difference compared to the corresponding control. EPAC: exchange protein directly activated by cAMP; cAMP: cyclic adenosine monophosphate; AE: acrosomal exocytosis; TG: thapsigargin.