Chronic nicotine administration significantly increased aortic intima-media thickness (69.75 vs 51.42 μm) and impaired aortic reactivity in rats.
Does chronic nicotine administration impair aortic reactivity and induce vascular remodelling in male Sprague-Dawley rats?
Chronic nicotine administration at a dosage equivalent to a light smoker induces vascular remodelling, impairs aortic reactivity, and causes oxidative imbalance in rats.
Absolute Event Rate: 69.75% vs 51.42%
p-value: p=<0.05
Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p 0.05). Nicotine-treated group showed significant (p 0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group (ED50=1.4410 5 M vs. 4.910 6 M) (p 0.05 0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group (ED50=6.1710 7 M vs. 2.8210 7 M) (p 0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p 0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.
Zainalabidin et al. (2014) studied Healthy (investigating nicotine-induced aortic remodelling) (n=12). Nicotine vs. 0.9% normal saline was evaluated on Aortic intima-media thickness (IMT) (p=<0.05). Chronic nicotine administration significantly increased aortic intima-media thickness (69.75 vs 51.42 μm) and impaired aortic reactivity in rats.