Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats  

作　　者：Tian-ying XU Xiao-hong LAN Yun-feng GUAN Sai-long ZHANG Xia WANG Chao-yu MIAO 

机构地区：[1]Department of Pharmacology, Second Military Medical University, Shanghai 200433, China [2]Department of Pharmacy, 81th Hospital of PLA, Nanjing 210002, China [3]Center of Stroke, Beijing Institute for Brain Disorders, Beijing 100069, China

出　　处：《Acta Pharmacologica Sinica》2015年第4期429-439,共11页中国药理学报（英文版）

基　　金：This work was supported by grants from the National Natural Science Foundation of China （No 81102487 to Tian- ying XU and 81130061 and 81373414 to Chao-yu MIAO）, and the National Science and Technology Major Project （No 2009ZX09303-002 to Chao-yu MIAO）.

摘　　要：Aim： To investigate the effect of chronic nicotine treatment on vascular function and to identify the underlying mechanisms. Methods： Adult rats were treated with nicotine （3 mg·kg^-1·d^-1, sc） for 6 weeks. After the rats were sacrificed, aortic rings were prepared for detecting vascular reactivity, and thoracic aorta and periaortic fat samples were collected for histological and molecular biology studies. Results： Chronic nicotine treatment significantly reduced periaortic fat, and specifically enhanced smooth muscle relaxation without altering the aortic adventitial fat and endothelium function. Pretreatment with the soluble guanylyl cyclase inhibitor ODQ （3 μmol/L） or PKG inhibitor Rp-8-Br-PET-cGMP （30 μmol/L） abolished the nicotine-induced enhancement of smooth muscle relaxation, whereas the cGMP analogue 8-Br-cGMP could mimic the nicotine-induced enhancement of smooth muscle relaxation. However, the chronic nicotine treatment did not alter PKG protein expression and activity in aortic media. Conclusion： Chronic nicotine treatment enhances vascular smooth muscle relaxation of rats via activation of PKG pathway.Aim： To investigate the effect of chronic nicotine treatment on vascular function and to identify the underlying mechanisms. Methods： Adult rats were treated with nicotine （3 mg·kg^-1·d^-1, sc） for 6 weeks. After the rats were sacrificed, aortic rings were prepared for detecting vascular reactivity, and thoracic aorta and periaortic fat samples were collected for histological and molecular biology studies. Results： Chronic nicotine treatment significantly reduced periaortic fat, and specifically enhanced smooth muscle relaxation without altering the aortic adventitial fat and endothelium function. Pretreatment with the soluble guanylyl cyclase inhibitor ODQ （3 μmol/L） or PKG inhibitor Rp-8-Br-PET-cGMP （30 μmol/L） abolished the nicotine-induced enhancement of smooth muscle relaxation, whereas the cGMP analogue 8-Br-cGMP could mimic the nicotine-induced enhancement of smooth muscle relaxation. However, the chronic nicotine treatment did not alter PKG protein expression and activity in aortic media. Conclusion： Chronic nicotine treatment enhances vascular smooth muscle relaxation of rats via activation of PKG pathway.

关 键 词：NICOTINE vascular smooth muscle nitric oxide cyclic GMP-dependent protein kinase type I ENDOTHELIUM VASODILATION NITROPRUSSIDE ACETYLCHOLINE adipose tissues 

分 类 号：Q463[生物学—生理学] Q421