As shown in panel A, the basal levels of amylase release was increased significantly jq1 in the presence of nico tine when compared to control levels and reduced signifi cantly in the presence of mecamylamine. Inhibitors,Modulators,Libraries Stimulation with CCK 8 enhanced the levels of amylase release in all groups. Treatment with nicotine induced CCK stimulated levels more than the control group. However, in the presence of mecamylamine, the enhanced response induced by nico tine was completely abolished returning the stimulated levels to that of control level. The response of acinar cell to amylase release by nicotine in the presence of conotoxin is identical to that of mecamylamine. Effect of H 7 or 2 APB on primary cell function, with or without nicotine The effects of nicotine in the presence or absence of H 7, and 2 APB on the basal and cell stimulated primary acinar cell function are shown in Figure 3.

Inhibitors,Modulators,Libraries The upper panel represents the basal and stimulated amylase re lease in the presence of H 7 while the lower panel represents the effect of 2 APB. As shown in panel A, the basal levels of amylase release were similar in all four groups. Stimulation with CCK 8 enhanced the levels of amylase release in all groups. Treatment with nicotine induced CCK stimulated levels more than the control group. However, in the presence of H 7, or 2 APB the enhanced response induced by nicotine was completely abolished and returned to stimulated value as of control. The response of acinar cell to amylase release by nicotine in the presence of H 7 is identical Inhibitors,Modulators,Libraries to that of 2 APB.

Effect of ERK and AKT Inhibitor on primary cell function with or without nicotine The effects Inhibitors,Modulators,Libraries of nicotine in the presence or absence of MAPK inhibitors, UO126, and AKT on the basal and cell stimulated primary acinar Inhibitors,Modulators,Libraries cell function are shown in Figure 4. The upper panel represents the basal and stimulated amylase release in the presence of AKT inhibitor while the lower panel represents the effect of UO126. As shown in panel A, the basal levels of amylase release were similar in all four groups. Upon stimulation with CCK 8, levels of amylase release were enhanced significantly in all groups in all groups. Treat ment with nicotine induced CCK stimulated levels more than the control group. However, in the presence of AKT inhibitor, or such UO126, the enhanced response induced by nicotine remained unaltered. The response of acinar cell to amylase release by nicotine in the pres ence of AKT inhibitor is identical to that of UO126. Effect of JNK inhibitor or p38 inhibitor on primary cell function, with or without nicotine The effects of nicotine in the presence or absence of MAPK inhibitors, JNK, and p38 kinase inhibitors on the basal and cell stimulated primary acinar cell function are shown in Figure 5.