title: Inhibition of inflammation contributes to organ protection of atenolol in sinoaortic-denervated rats.
abstract: The present study was designed to test the hypothesis that inhibition of inflammation contributes to the protective effects of atenolol on the organ damage induced by sinoaortic denervation (SAD) in rats. SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Atenolol (20 mg/kg/d, po) was administered for 12 weeks beginning from 4 weeks after SAD. Organ damage evaluation and the determination of plasma TXB2, serum IL-1, TNF-alpha and tissue reactive oxygen species (ROS) were performed at 16 weeks after SAD. It was found that there existed obvious organ damage including increased cardiac and aortic collagen, and glomerular injury, in SAD rats. Plasma TXB2, serum TNF-alpha IL-1, and tissue ROS increased significantly after SAD. Long-term treatment with atenolol significantly prevented the organ damage with a decrease in left ventricular weight, cardiac and aortic collagen contents, and glomerular injury score in SAD rats. Plasma TXB2, serum IL-1, and tissue ROS were found to be significantly decreased by the long-term treatment with atenolol. Furthermore, it was found that the levels of inflammation-related factors were significantly related to all the organ-damage parameters studied in this experiment. These results suggest that inhibition of inflammation and oxygen stress contributes to the organ-protective effects of atenolol in SAD rats.
authors.affiliation: Department of Pharmacology, Second Military Medical University, Shanghai, China.
authors.forename: Chuan
authors.initials: C
authors.lastname: Zhang
authors.forename: He-Hui
authors.initials: HH
authors.lastname: Xie
authors.forename: Ze-An
authors.initials: ZA
authors.lastname: Lu
authors.forename: Min-Juan
authors.initials: MJ
authors.lastname: Zhu
authors.forename: Ding-Feng
authors.initials: DF
authors.lastname: Su
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000494:pharmacology*; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D001262:Atenolol / Q000008:administration & dosage / Q000494:pharmacology*; D003094:Collagen / Q000378:metabolism; D003714:Denervation; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control*; D007375:Interleukin-1 / Q000097:blood; D007668:Kidney / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012849:Sinoatrial Node / Q000294:innervation*; D013929:Thromboxane B2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000959:Antihypertensive Agents; D007375:Interleukin-1; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D001262:Atenolol; D013929:Thromboxane B2; D003094:Collagen