Figure 7.

Dose-dependent acetylcholine chloride (Ach)- and nicotine-evoked catecholamine secretion and blockade by hexamethonium. (A) Individual slices were stimulated for 5 min by either ACh (10 and 100 µM) or nicotine (1, 3, 10, and 100 µM). Both E [(A), a] and norepinephrine (NE) [(A), b] release dose-dependently increases with agonist concentration. Note that for a same agonist concentration, nicotine is more efficient to evoke E and NE secretion [(A), c]. (B) Effect of the α3-containing nAChR antagonist hexamethonium. Slices were incubated for 5 min with hexamethonium (200 µM) before challenging with 10 µM nicotine (or saline for control experiments). While basal E and NE secretion is not affected by hexamethonium, nicotine-triggered E [(B), a] and NE [(B), b] release is significantly reduced. [(B), c] Pooled data illustrating a strongest ability for hexamethonium to reduce NE secretion compared to E secretion (88 versus 57% decrease). *p < 0.05, **p < 0.01, ***p < 0.001.