title: Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Chronic nicotine treatment enhances vascular smooth muscle relaxation of rats via activation of PKG pathway.
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai 200433, China.
authors.forename: Tian-ying
authors.initials: TY
authors.lastname: Xu
authors.affiliation: 1] Department of Pharmacology, Second Military Medical University, Shanghai 200433, China [2] Department of Pharmacy, 81th Hospital of PLA, Nanjing 210002, China.
authors.forename: Xiao-hong
authors.initials: XH
authors.lastname: Lan
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai 200433, China.
authors.forename: Yun-feng
authors.initials: YF
authors.lastname: Guan
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai 200433, China.
authors.forename: Sai-long
authors.initials: SL
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai 200433, China.
authors.forename: Xia
authors.initials: X
authors.lastname: Wang
authors.affiliation: 1] Department of Pharmacology, Second Military Medical University, Shanghai 200433, China [2] Center of Stroke, Beijing Institute for Brain Disorders, Beijing 100069, China.
authors.forename: Chao-yu
authors.initials: CY
authors.lastname: Miao
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000502:physiology; D062965:Cyclic GMP-Dependent Protein Kinase Type I / Q000378:metabolism; D005223:Fats / Q000378:metabolism; D005731:Ganglionic Stimulants / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009538:Nicotine / Q000008:administration & dosage / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D005223:Fats; D005731:Ganglionic Stimulants; D018722:Nicotinic Agonists; D009538:Nicotine; D062965:Cyclic GMP-Dependent Protein Kinase Type I
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