title: The ameliorating effects of long-term electroacupuncture on cardiovascular remodeling in spontaneously hypertensive rats.
abstract: BACKGROUND
  The purpose of this study was to investigate the inhibitory effects of long-term electroacupuncture at BaiHui (DU20) and ZuSanLi (ST36) on cardiovascular remodeling in spontaneously hypertensive rats (SHR) and underlying mechanisms.
  
  
  METHODS
  6-weeks-old SHR or Wistar male rats were randomly, divided into 6 groups: the control group (SHR/Wistar), the non-acupoint electroacupuncture stimulation group (SHR-NAP/Wistar-NAP) and the electroacupuncture stimulation at DU20 and ST36 group (SHR-AP/Wistar-AP), 24 rats in each group. Rats were treated with or without electroacupuncture at DU20 and ST36, once every other day for a period of 8 weeks. The mean arterial pressure (MAP) was measured once every 2 weeks. By the end of the 8th week, the left ventricular structure and function were assessed by echocardiography. The content of angiotensin II (Ang II), endothelin-1 (ET-1) and nitric oxide (NO) in the plasma was determined using enzyme-linked immunosorbent assay. Histological studies on the heart and the ascending aorta were performed. The expression of angiotensin II type 1 receptor (AT1R), endothelin-1 type A receptor (ETAR), eNOS and iNOS in rat myocardium and ascending aorta was investigated by Western blotting.
  
  
  RESULTS
  The MAP in SHR increased linearly over the observation period and significantly reduced following electroacupuncture as compared with sham control SHR rats, while no difference in MAP was observed in Wistar rats between electroacupuncture and sham control. The aortic wall thickness, cardiac hypertrophy and increased collagen level in SHR were attenuated by long term electroacupuncture. The content of Ang II, ET-1 in the plasma decreased, but the content of NO increased after electroacupuncture stimulation in SHR. Long term electroacupuncture significantly inhibited the expression of AT1R, ETAR and iNOS, whereas increased eNOS expression, in myocardium and ascending aorta of SHR.
  
  
  CONCLUSIONS
  The long term electroacupuncture stimulation at DU20 and ST36 relieves the increased MAP and cardiovascular abnormality in both structure and function in SHR, this beneficial action is most likely mediated via modulation of AT1R-AT1R-ET-1-ETAR and NOS/NO pathway.
authors.forename: Ze-Jun
authors.initials: ZJ
authors.lastname: Huo
authors.forename: Quan
authors.initials: Q
authors.lastname: Li
authors.forename: Gui-Hua
authors.initials: GH
authors.lastname: Tian
authors.forename: Chang-Man
authors.initials: CM
authors.lastname: Zhou
authors.forename: Xiao-Hong
authors.initials: XH
authors.lastname: Wei
authors.forename: Chun-Shui
authors.initials: CS
authors.lastname: Pan
authors.forename: Lei
authors.initials: L
authors.lastname: Yang
authors.forename: Yan
authors.initials: Y
authors.lastname: Bai
authors.forename: You-Yi
authors.initials: YY
authors.lastname: Zhang
authors.forename: Ke
authors.initials: K
authors.lastname: He
authors.forename: Chuan-She
authors.initials: CS
authors.lastname: Wang
authors.affiliation: Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing, China. lizhglq620@163.com.
authors.forename: Zhi-Gang
authors.initials: ZG
authors.lastname: Li
authors.forename: Jing-Yan
authors.initials: JY
authors.lastname: Han
mesh_terms: D015669:Acupuncture Points; D000804:Angiotensin II / Q000097:blood / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology*; D001794:Blood Pressure; D006332:Cardiomegaly / Q000628:therapy*; D003094:Collagen / Q000378:metabolism; D015671:Electroacupuncture; D019332:Endothelin-1 / Q000097:blood / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006973:Hypertension / Q000097:blood / Q000628:therapy*; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009569:Nitric Oxide / Q000097:blood; D019001:Nitric Oxide Synthase / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000097:blood / Q000378:metabolism; D066253:Vascular Remodeling
chemical_list: D019332:Endothelin-1; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D009569:Nitric Oxide; D003094:Collagen; D019001:Nitric Oxide Synthase