par Adamopoulos, Dionysios 
;Van De Borne, Philippe ;Argacha, Jean-François
Référence Clinical and experimental pharmacology & physiology, 35, 4, page (458-463)
Publication Publié, 2008-04
;Van De Borne, Philippe ;Argacha, Jean-François Référence Clinical and experimental pharmacology & physiology, 35, 4, page (458-463)
Publication Publié, 2008-04
Article révisé par les pairs
| Résumé : | 1. Nicotine is a well studied pleiotropic agent which occurs naturally in tobacco smoke and has been largely accused for many of the adverse effects of smoking on the cardiovascular system, including autonomic imbalance, endothelial dysfunction and coronary blood flow dysregulation. 2. The acute sympathoexcitatory effects of smoking on the cardiovascular system are partially mediated by catecholamine release, muscle sympathetic nerve excitation and peripheral chemoreceptor sensitivity increase, consecutive to nicotinic receptor stimulation in the autonomic nervous system. 3. Recent animal data suggest that nicotine promotes the oxidative and inflammatory stress to the endothelium and induces pathological angiogenesis, leading to the progression of the atherosclerotic lesions. 4. Nicotine increases myocardial work without impairing the physiological coronary vasodilatation. Consequently, nicotine per se cannot explain the sudden reduction in coronary flow reserve after exposure to both active and passive smoking. 5. Nicotine's biological effects are characterized by a rapid onset of tolerance, which can explain why nicotine administration does not elicit acute coronary and chemoreflex side-effect in smokers. |
