Nicotine: a pro-angiogenic factor.

Angiogenesis, the formation of new blood vessels from pre-existing ones, is regulated by the balance between angiogenic activating and inhibiting factors. Recent evidence indicates that nicotine, an alkaloid compound, presents pro-angiogenic effects in certain concentrations. Nicotine-induced angiogenesis results from the stimulation of non-neuronal nicotinic acetylcholinergic receptors (particularly alpha 7-NAChR subtype) and involves growth factor secretion and activation of intracellular signalling pathways. Although nicotine is a constituent of tobacco smoke, its contribution towards pathophysiology of several tobacco-associated pathologies is controversial. Nowadays, nicotine is used in tobacco smoke cessation programs, but, again, its use is still a matter of discordance regarding cardiovascular morbidity. Nevertheless, given the established effects of nicotine-induced angiogenesis, this alkaloid might be of therapeutic value in situations of inefficient angiogenesis, such as peripheral vascular impairment and tissue ischemia. Conversely, blockade of nicotine pathway can be helpful in complications exhibiting excessive angiogenesis, namely in diabetic retinopathy and nephropathy or neoplasia. Knowing that nicotine is involved in many angiogenic-associated disorders with a high prevalence in the western world, and that this alkaloid widely used in smoke cessation programs, elucidation of the action of nicotine on the vascularization process is of utmost importance. The current paper provides an overview of the effects of nicotine in angiogenesis.