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We hypothesize that nicotine impairs \u03b2 adrenergic\u2013mediated cAMP signaling in VSM, leading to altered vascular reactivity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The effects of nicotine on cAMP signaling and vascular function were systematically tested in aortic VSM cells and acutely isolated aortas from mice expressing the cAMP sensor <jats:sup>T<\/jats:sup>Epac<jats:sup>VV<\/jats:sup> (Camper), specifically in VSM (e.g., Camper<jats:sub>SM<\/jats:sub>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Isoproterenol (ISO)\u2010induced \u03b2\u2010adrenergic production of cAMP in VSM was significantly reduced in cells from second\u2010hand smoke (SHS)\u2013exposed mice and cultured wild\u2010type VSM treated with nicotine. The decrease in cAMP synthesis caused by nicotine was verified in freshly isolated arteries from a mouse that had cAMP sensor expression in VSM (e.g., Camper<jats:sub>SM<\/jats:sub> mouse). Functionally, the changes in cAMP signaling in response to nicotine hindered ISO\u2010induced vasodilation, but this was reversed by immediate PDE3 inhibition.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results imply that nicotine alters VSM \u03b2 adrenergic\u2013mediated cAMP signaling and vasodilation, which may contribute to the dysregulation of vascular reactivity and the development of vascular complications for nicotine\u2010containing product users.<\/jats:p><\/jats:sec>","DOI":"10.1111\/micc.12871","type":"journal-article","created":{"date-parts":[[2024,5,28]],"date-time":"2024-05-28T18:13:03Z","timestamp":1716919983000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Nicotine Impairs Smooth Muscle <scp>cAMP<\/scp> Signaling and Vascular 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