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. 2003 Mar 26;138(6):1031–1035. doi: 10.1038/sj.bjp.0705171

Figure 2.

Figure 2

(a) Effects of apamin and ChTX on EDHF relaxations induced by ACh in arteries precontracted with phenylephrine (PE). ChTX alone (50 nM; n=6) and apamin alone (50 nM; n=6) were without significant effect on EDHF relaxations. ChTX and apamin in combination (each 50 nM; n=6) abolished EDHF-mediated relaxation. Data are means ± s.e.mean. (b) Continuous recording of endothelial cell membrane potential (Em). Apamin and MTX in combination completely, and reversibly, abolished the hyperpolarization to ACh (10 μM). (c) Representative trace to demonstrate concentration-dependent relaxation to ACh (0.01–10 μM) in precontracted arteries. (d) and (e) Representative traces demonstrating concentration-dependent relaxation to ACh (0.01–10 μM) in the presence of apamin (50 nM) and MTX (50 nM), respectively. (f) Representative record to demonstrate abolition of relaxation in the presence of apamin and MTX. The ability of the smooth muscle to relax in the presence of the toxin combination was demonstrated by maximal relaxation to levcromakalin (lev; 10 μM). As evidenced on original traces, relaxations to lower concentrations of ACh were transient. For the construction of concentration–effect curves, the maximal relaxations to each applied dose of ACh were recorded.