Nicotine and Cardiovascular Function

Nicotine is a natural alkaloid of tobacco leaves that specifically interacts with a cholinergic receptor (AChR) population which is therefore AU4 pharmacologically identified as nicotinic (nAChR). By virtue of that, nicotine is able to affect the function of those tissues expressing nAChR, particularly the brain, where it develops substance dependence, and the heart. Effects on the heart depend on multiple mechanisms of action involving regulatory centers in the brainstem that control the sympathetic outflow, although most of the effects on heart rate and blood pressure depend upon the direct ganglionic stimulation leading to the release of catecholamines in blood by adrenal glands. Nonetheless, Nicotine is able to interact directly with ion channels of cardiomyocytes involved in the development of the action potential, as well as with inflammatory cells involved in cardiac fibrosis and remodeling. Understanding its multiple intimate relationships with human physiology is necessary in order to develop effective pharmacological strategies based on the use of partial agonists aimed at contrasting addiction, thereby preventing nicotine toxicity.