The Effects of Nicotine on Cardiac Function and Structure

Abstract

Nicotine is the addictive chemical in tobacco‐related products, such as cigarettes, water pipes, e‐cigs, and chewing tobacco. While the effects of smoke from cigarettes and cigars are well known, the rise in popularity of smokeless electronic cigarettes (e‐cigs) brings new questions about the effects of nicotine itself on the development of cardiovascular disease. These “smoke‐less” products have grown in popularity due to reduced costs, increased social acceptance, and a belief that e‐cigs are a less dangerous alternative to smoking.Nicotine use is associated with hypertension and may activate the renin‐angiotensin system when inhaled. The renin‐angiotensin system regulates blood pressure, and a major component of the system, angiotensin‐II (Ang‐II), can cause cardiac hypertrophy and fibrosis. However, most animal studies administer nicotine via infusion, and very little is known about the effects of chronically inhaled nicotine.Thus the goal of our study is to investigate the effects of chronic inhaled nicotine on cardiac function and structure.C57BL/6 male mice aged 8–12 weeks were used in this study. Mice were exposed to nicotine vapor in their home cage using an exposure system that provides control of chronicity and nicotine dosing. Mice were exposed for 12 hours/day corresponding with the dark cycle. Following 4 weeks of either nicotine or air exposure, subsets of these groups were implanted with osmotic mini‐pumps containing Ang‐II to induce hypertrophy and fibrosis. Cardiac function was assessed by ultrasound echocardiography and tissue samples collected for protein and mRNA analysis. While there was no significant change in left ventricular function, we found that nicotine blunted Ang‐II mediated hypertrophy in the posterior wall (0.83 ± 0.03 mm, n=19) compared to Ang‐II exposed mice (0.93 ± 0.02 mm, n=19, p< 0.01). While there were no differences in collagen 1 and 3 mRNA expression between groups, our preliminary data showed an increase in collagen I protein expression in nicotine exposed mice compared to air controls (1.27 ± 0.05 vs. 1 ± 0.09, n=2–3 respectively).In conclusion, while nicotine does not appear to affect left ventricular cardiac function, nicotine does blunt Ang‐II mediated hypertrophy. In addition, there is also evidence for increased cardiac collagen deposition in nicotine exposed mice. Future studies to measure right ventricular function, cardiomyocyte size, hypertrophic pathways, and cardiac fibroblast activity are in progress.Support or Funding InformationNHLBI R01 HL135635NIH Grant #R25GM121189This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.