Nicotine enhances murine airway contractile responses to kinin receptor agonists via activation of JNK- and PDE4-related intracellular pathways

Table 3 Effects of nicotine on endothelin receptor-mediated airway contractions

Incubation time	Nicotine (μM)		ET_A			ET_B
		n	E _max (mN)	pEC ₅₀	n	E _max (mN)	pEC ₅₀
Day 1	0 (Ctrl)	10	3.61 ± 0.40	7.52 ± 0.14	9	3.49 ± 0.68	8.00 ± 0.13
	10	10	3.40 ± 0.33	7.50 ± 0.07	10	3.52 ± 0.53	7.89 ± 0.07
Day 2	0 (Ctrl)	4	3.74 ± 0.87	7.40 ± 0.20	4	3.33 ± 0.34	8.24 ± 0.13
	10	4	4.22 ± 0.85	7.52 ± 0.11	4	3.15 ± 0.60	8.00 ± 0.13
Day 4	0 (Ctrl)	9	4.32 ± 0.71	7.81 ± 0.10	9	4.31 ± 0.73	8.05 ± 0.09
	1	9	4.13 ± 0.42	7.74 ± 0.07	9	4.03 ± 0.46	8.17 ± 0.13
	10	8	4.67 ± 0.37	7.86 ± 0.10	8	4.47 ± 0.38	8.18 ± 0.12

Tracheal segments were cultured for 1, 2 or 4 days in presence of vehicle (0.1% DMSO, Ctrl) or nicotine (1 or 10 μM). ET_A: endothelin receptor type A; ET_B: endothelin receptor type B. Responses of ET_B receptors were tested with the selective ET_B agonist sarafotoxin 6c, while responses to ET_A receptors were tested with the non-selective ET-receptor agonist sarafotoxin 6b after the desensitization of ET_B receptors [39]. E_max and pEC₅₀ are presented as mean ± S.E.M. Statistical analysis was performed using unpaired student's t-test with Welch's correction. Nicotine vs Ctrl (DMSO). No significant differences were found between the two groups. n = number of experiments performed.

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