![]() ![]() ![]() for 8 weeks) failed to develop an increased RVSP (24.0 ± 1.3 mmHg, n=12). In addition, mice exposed to nicotine and treated concomitantly with losartan (10 mg/kg/day s.c. the air controls, P < 0.05) and enhanced activation of mitogen-activated protein kinase pathways including ERK, p38 and JNK in the RV, but not in the LV, following chronic nicotine inhalation exposure. Mechanistically we observed increased expression of angiotensin converting enzyme (3.87-fold increase in nicotine-exposed mice vs. In the lung, there was a 1.50-fold increase in the number of muscularized pulmonary arterioles in nicotine-exposed mice compared to air-exposed mice ( P < 0.001), concomitant with increased pulmonary vascular resistance (1.41 ± 0.22 mmHg In contrast, there were no significant structural or functional changes in the left ventricle (LV) following nicotine exposure. 0.42 ± 0.03 mm in air control group, P < 0.05) and a trend of increase in RV internal diameter (1.92 ± 0.21 mm in nicotine group vs. Echocardiography showed that 8-week nicotine inhalation resulted in RV hypertrophy with increased RV free wall thickness (0.50 ± 0.02 mm in nicotine group vs. ![]() At 8 weeks, significantly increased RVSP was detected in nicotine-exposed mice (39.6 ± 4.2 mmHg, n=7) compared to the air controls (22.3 ± 1.7 mmHg, n=8, P < 0.01). Nicotine-exposed mice exhibited elevated systemic BP from weeks 1–3, which then returned to baseline from weeks 4–8, indicating development of tolerance to nicotine. At the end of the 8 weeks, mice were subjected to right heart catheterization to measure right ventricular systolic pressure (RVSP). Systemic BP was recorded weekly by radio-telemetry and cardiac remodeling was monitored by echocardiography. Nicotine exposure was assessed by weekly measurement of serum cotinine levels, which showed a weekly average of 599.0 ± 54.3 ng/ml in nicotine-exposed mice. Male C57BL6/J mice were exposed to air (control) or nicotine vapor (daily, 12 h on/12 h off) for 8 weeks. The purpose of this study was to examine the effects of chronic nicotine inhalation on the development of CVPD with a focus on blood pressure (BP) and cardiac remodeling. Cigarette smoking is the single most important risk factor for the development of cardiovascular and pulmonary diseases (CVPD), however, the role of nicotine in the pathogenesis of CVPD is incompletely understood. ![]()
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