Effects of cigarette smoking on metabolic events in the lung.

Abstract

Nicotine and cigarette smoke extract show acute physiological effects: increasing tracheal pressure (PTR), pulmonary artery pressure (PPA), systemic blood pressure (PyT), and left atrium pressure (PLA); and decreasing cardiac output (4AORTA) and blood flow to the left lower lobe (1L). In addition, cigarette smoking induces bronchoconstriction, thus decreasing peak flow, FVC, and FEVY.o in healthy subjects. It has also been demonstrated that cigarette smoking caused temporary slowing of mucociliary clearance in the lung and that cigarette smoke increases the activity of aryl hydrocarbon hydroxylase which metabolizes benzo [a]pyrene. We demonstrated that serum angiotensin I converting enzyme (ACE) activity showed a significant increase immediately after smoking and returned to the control level 20 min after smoking. We also demonstrated that plasma histamine levels showed a marked decrease after smoldng. Furthermore, the effects of cigarette smoke and related substances on prostaglandin, thromboxane, testosterone, cyclic nucleotides metabolism, and protein synthesis were also investigated.

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

“…Several studies have observed that angiotensin II promotes inflammation and tissue injury, mediating key events in animal models of autoimmune disease (Marchesi, Paradis, & Schiffrin, 2008; Okunuki et al., 2009; Platten et al., 2009; Sagawa, Nagatani, Komagata, & Yamamoto, 2005; Stegbauer et al., 2009). Based on previous observations demonstrating that serum ACE activity increases significantly after smoking (Kitamura, 1987) and chronic smoking results in enhanced RAS activation in monozygotic twins, discordant for smoking (Laustiola, Lassila, & Nurmi, 1988), Correale and Farez (2015) (Correale & Farez, 2015) recently investigated whether RAS might be involved in immunomodulatory effects of smoking on MS progression. As expected, their findings argue in favor of smoking having modulator role in the expression and activity of RAS components: both auto‐reactive T‐lymphocytes and monocytes derived from patients who smoked produced significantly higher amounts of renin, ACE, as well as angiotensin II receptor type I (AT1R).…”

Nicotine and the renin-angiotensin system

“…This increase, however, was not sustained after repeated 10-day exposure, indicating a time-or exposure (acute vs. chronic)-dependent effect (7). In healthy human volunteers, serum ACE activity showed a significant increase immediately after smoking and returned to control level 20 min after smoking (80). Increased serum ACE levels were also found in dogs after exposure to cigarette smoke or intravenous nicotine infusion (126).…”

“…Studies in laboratory animals support the activation of RAS by cigarette smoke or nicotine. Chronic nicotine administration through osmotic minipumps has been shown to elevate plasma renin activity in rats subjected to a high-salt diet (120), and cigarette smoke and/or nicotine administration increase plasma ACE activity with increased conversion of ANG I to ANG II (7,80,126).…”

Efek akut merokok kretek terhadap fungsi ventrikel kanan

“…Aktivitas angiotensin converting enzim (ACE) juga meningkat dan kembali ke kontrol dalam dua puluh menit. [30][31][32][33] Patogenesis rokok dalam hubungannya dengan peninggian tekanan arteri pulmonal diinvestigasi oleh Wright 18,19 Barutcu et al 15 juga melaporkan dari 20 perokok yang dievaluasi dengan Doppler serta tricuspid inflow and early and late velocity didapatkan penurunan indeks performa ventrikel kanan sebelum dan 30 menit sesudah merokok.…”