Figure 2
The role of membrane potential (Em) depolarization and voltage-gated Ca2+ channels in 5-hydroxytryptamine (5-HT)-induced mesenteric artery constriction. (a) A typical trace of mesenteric artery constriction in response to cumulative concentrations of 5-HT. (b) The effect of high KCl (70 mM) pretreatment on 5-HT-induced mesenteric artery constriction. (c) The effects of nifedipine (1 μM) on 5-HT-induced constriction. (d) The effects of the combined treatment of high KCl (70 mM) and nifedipine (1 μM) on 5-HT-induced constriction. (e) Concentration–response curves for 5-HT-induced vasoconstriction under the conditions described in (a–d); both high KCl (70 mM) and nifedipine (1 μM) pretreatment markedly suppressed 5-HT-induced mesenteric artery constriction. High KCl-induced vasoconstriction is shown (a, c) before breaks for comparison with 5-HT-induced constriction. The duration of high-KCl treatment was 10 min (note that the timescale bars are for traces after the break). **P<0.01 and ***P<0.001 versus the control. NS, not significant between all data points between the two groups.
