Aortic Remodelling in Chronic Nicotine-Administered Rat

Abstract

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.

Lactobacillus caseistrain C1 attenuates vascular changes in spontaneously hypertensive rats

“…Reactivity towards vasoconstrictor agonist, PE, and endothelium-dependent vasorelaxant agonist, ACh, determines sensitivity of the aorta [11]. Hypertension causes relatively high aorta contractility but low aorta relaxation in response to PE and ACh, respectively.…”

“…Structural remodeling is often coupled with impaired vascular reactivity. This phenomenon was clearly demonstrated in rats undergoing chronic nicotine administration [11]. One of the key factors that results in hypertensive vessels and impaired vascular reactivity is low bioavailability of nitric oxide (NO) [12].…”

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

“…This supports the theory that nicotine may chronically alter aortic distensibility. Indeed, in vitro models have shown that nicotine alone has aortic-remodeling properties and may alter smooth muscle cells from contractile to synthetic type [184,185].…”

Angiotensin II Type I Receptor Antagonism Attenuates Nicotine-Induced Cardiac Remodeling, Dysfunction, and Aggravation of Myocardial Ischemia-Reperfusion Injury in Rats

“…Prolonged exposure to nicotine via cigarette smoking, chewable tobacco, as well as nicotine inhalation devices is associated with an increased risk of cardiovascular diseases (McEvoy et al, 2015;Kim et al, 2017;Kunutsor et al, 2018). In animal models, prolonged administration of nicotine not only promotes vascular endothelial dysfunction associated with hypertension, but also directly impacts the cardiac structure and function, promoting oxidative stress, inflammation, fibrosis, and cardiomyocyte apoptosis (Joukar et al, 2012;Zainalabidin et al, 2014;Ramalingam et al, 2016;Si et al, 2017a;Li et al, 2018). In several lines of evidence, nicotine was shown to induce cardiac damage independent of hypertension, directly accounting for significant reduction in cardiac function (Hu et al, 2011).…”