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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 3. Chronic nicotine inhalation impairs endothelium-dependent vasodilation of thoracic aorta in wild-type but not α7-nAChR−/− male mice.

Figure 3.

(A) Thoracic aortas isolated from wildtype male mice exposed to nicotine (n=12) exhibit reduced vasodilatory response to acetylcholine (ACh) compared with those from air-exposed males (n=11); *P<0.05, **P<0.01. The EC50 of ACh was not impacted by nicotine and is represented for each response curve as a dashed vertical line. (B and C) Chronic nicotine inhalation does not alter vasodilatory response to sodium nitroprusside (SNP) or vasoconstrictive response to phenylephrine (Phe) in thoracic aorta. Air, n=9–11; nicotine, n=10–12. (D–F) Thoracic aortas isolated from α7-nAChR−/− male mice exposed to nicotine (n=3–7) and air (n=3–6) 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.