Aortic Remodelling in Chronic Nicotine-Administered Rat

• 영문명: Aortic Remodelling in Chronic Nicotine-Administered Rat
• 발행기관: 대한생리학회-대한약리학회
• 저자명: Satirah Zainalabidin Siti Balkis Budin An Ramalingam Yi Cheng Lim
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제18권 제5호, 411~418쪽, 전체 8쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2014.01.01

영문 초록

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=1.44×10⁵ M vs. 4.9×10⁶ 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=6.17×10⁷ M vs. 2.82×10⁷ 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.

키워드

Aorta Nicotine Oxidative Stress Reactivity Remodelling