Abstract
Exposure to cigarette smoke is an important risk factor for cardiovascular diseases. Nicotine is an addictive compound in cigarette smoke that triggers oxidative stress, which leads to vascular dysfunction. Piper sarmentosum Roxb. is a herb with antioxidant and vascular protective effects. This study evaluated the potential protective effect of the aqueous extract of P. sarmentosum leaf (AEPS) on vascular dysfunction in rats induced with prolonged nicotine administration. A total of 22 male Sprague-Dawley rats were divided into control (normal saline, oral gavage [p.o.]), nicotine (0.8 mg/kg/day nicotine, intraperitoneally [i.p.]), and nicotine + AEPS groups (250 mg/kg/day AEPS, p.o. + 0.8 mg/kg/day nicotine, i.p.). Treatment was given for 21 days. Thoracic aortae were harvested from the rats for the measurement of vasorelaxation, vascular nitric oxide (NO) level, and antioxidant level and the assessment of vascular remodeling. Rats treated with AEPS had improved vasorelaxation to endothelium-dependent vasodilator, acetylcholine (ACh), compared with the nicotine-induced rats (p < 0.05). The presence of endothelium increased the maximum relaxation of aortic rings in response to ACh. Compared with the nicotine group, AEPS enhanced vascular NO level (p < 0.001) and increased antioxidant levels as measured by superoxide dismutase activity (p < 0.05), catalase activity (p < 0.01), and reduced glutathione level (p < 0.05). No remarkable changes in aortic histomorphometry were detected. In conclusion, P. sarmentosum attenuates vascular endothelial dysfunction in nicotine-induced rats by improving vasorelaxation and enhancing vascular NO and antioxidant levels.
Highlights
Tobacco smoking contributes to eight million of annual deaths worldwide
No remarkable difference was observed in vasorelaxation toward endothelium-independent vasodilator, sodium nitroprusside (SNP), in all groups (Figures 1C,D)
ACh works by binding to M3 receptors on the endothelium, which leads to calcium release and endothelial nitric oxide synthase activation. eNOS converts L-arginine to NO, which diffuses from the endothelial cells (EC) into the adjacent layer of smooth muscle to cause vasorelaxation (Sandoo et al, 2010)
Summary
Tobacco smoking contributes to eight million of annual deaths worldwide. More than seven million deaths are attributed to the direct effects of smoking, and more than 1.2 million premature deaths of adults and children due to exposure to secondhand smoke have been recorded annually (World Health Organization, 2019). Tobacco smoking and exposure to nicotine increase the risk of cardiovascular diseases (CVD), such as atherosclerosis, ischemic heart disease, hypertension, and stroke (Son and Lee, 2020). The effect of nicotine on the cardiovascular system is mediated by its binding to endogenous nicotinic acetylcholine receptors (nAChRs). NAChRs are expressed by vascular endothelial cells (EC) and vascular smooth muscle cells (VSMC); ECs and VSMCs are the direct targets of nicotine-induced vascular dysfunction (Brüggmann et al, 2003; Moccia et al, 2004). The presentations of nicotine-induced vascular dysfunction include changes in vasoreactivity and vascular remodeling (Whitehead et al, 2021)
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