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. Author manuscript; available in PMC: 2023 Jun 30.
Published in final edited form as: Clin Sci (Lond). 2022 Jun 30;136(12):973–987. doi: 10.1042/CS20220083

Figure 4. Chronic nicotine inhalation impairs vasoreactivity of pulmonary artery in wild-type but not α7-nAChR−/− male mice.

Figure 4.

(A) Pulmonary arteries isolated from wild-type male mice exposed to nicotine (n=10) exhibit reduced vasodilatory response to acetylcholine (ACh) compared with those exposed to air (n=10); **P<0.01. The EC50 of ACh was significantly increased by nicotine and is represented for each response curve as a dashed vertical line; †P<0.05. (B) Pulmonary arteries isolated from wild-type male mice exposed to nicotine (n=6) exhibit similar vasodilatory response to sodium nitroprusside (SNP) compared with those exposed to air (n=6). (C) Pulmonary arteries isolated from wild-type male mice exposed to nicotine (n=10) exhibit enhanced vasoconstrictive response to phenylephrine (Phe) compared with those exposed to air (n=10), and pretreatment with L-NAME (10 μM) abolishes the heightened response (right, n=9/group); *P<0.05. (D–F) Pulmonary arteries isolated from α7-nAChR−/− male mice exposed to nicotine (n=7–8) and air (n=5–6) exhibit similar vasoreactivity to ACh, SNP, and Phe. Response curves were analyzed by two-way ANOVA followed by Bonferroni’s multiple comparisons test and EC50 was analyzed by two-tailed Student’s t-test.