Perinatal nicotine/smoking exposure and carotid chemoreceptors during development

Tobacco smoking is still a common habit during pregnancy and is the most important preventable cause of many adverse perinatal outcomes. Prenatal smoking exposure can produce direct actions of nicotine in the fetus with the disruption of body and brain development, and actions on the maternal–fetal unit by causing repeated episodes of hypoxia and exposure to many toxic smoke products (such as carbon monoxide). Specifically, nicotine through binding to nicotinic acetylcholine receptors have ubiquitous effects and can affect carotid chemoreception development through structural, functional and neuroregulatory alterations of the neural circuits involved in the chemoafferent pathway, as well as by interfering with the postnatal resetting of the carotid bodies. Reduced carotid body chemosensitivity and tonic activity have thus been reported by the majority of the human and animal studies. This review focuses on the effects of perinatal exposure to tobacco smoke and nicotine on carotid chemoreceptor function during the developmental period. A description of the effects of smoking and nicotine on the control of breathing related to carotid body activity, and of the possible physiopathological mechanisms at the origin of these disturbances is presented.