How does nicotine increase atherosclerosis?

Nicotine is known to have several adverse effects on the cardiovascular system, and one of its critical mechanisms in increasing the risk of atherosclerosis is through the release of epinephrine and norepinephrine. These substances are catecholamines that, when released in response to nicotine, lead to vasoconstriction, increased heart rate, and elevated blood pressure.

When nicotine stimulates the adrenal medulla, it promotes the release of these hormones into the bloodstream. This cascade not only momentarily increases cardiac workload but also contributes to endothelial injury and dysfunction over time, which are essential precursors to atherosclerosis.

The process of atherosclerosis is characterized by the buildup of plaques within the arterial walls, and the increased levels of stress on the cardiovascular system from the effects of epinephrine and norepinephrine can accelerate this process. Moreover, the persistent state of increased sympathetic nervous system activity can promote inflammation and enhance the formation of atherosclerotic plaque.

Understanding nicotine's impact on the cardiovascular system helps in addressing smoking cessation and the importance of reducing cardiovascular risk factors, as its effects extend beyond mere vasoconstriction to long-term progression of atherosclerotic disease.