title: Voluntary running exercise attenuates the progression of endothelial dysfunction and arterial calcification in ovariectomized rats.
abstract: OBJECTIVE
  Loss of oestrogen synthesis capacity after menopause contributes to increases in arterial stiffness and calcification. Exercise training improves arterial stiffness and calcification. However, the mechanism of exercise training-induced improvement of arterial stiffness and calcification remains unclear.
  
  
  METHODS
  We examined the mechanism by using aortas of sham-operated rats (sham control; SC), ovariectomized rats (OVX control; OC), OVX plus treatment with vitamin D(3) plus nicotine (VDN) rats (OV sedentary; OVSe), which is an animal model of endothelial dysfunction and arterial calcification, and voluntary running wheel exercise for 8 weeks plus OVX plus VDN rats (OV exercise; OVEx).
  
  
  RESULTS
  The arterial tissue calcium and endothelin-1 (ET-1: a vasoconstrictor peptide and a potent regulator of arterial calcification) levels were significantly higher in OVSe rats compared with the SC and OC rats, whereas these levels in the OVEx rats were significantly lower than in the OVSe rats. Additionally, arterial expression of endothelial nitric oxide synthase (eNOS), which is an enzyme that produces nitric oxide (NO: a vasodilator substance), was reduced in OVSe rats. However, exercise training prevented the decrease in eNOS expression. Moreover, there was a significant positive correlation between arterial calcium level and arterial ET-1 level.
  
  
  CONCLUSIONS
  These findings suggest that exercise training-induced improvement of ET-1 and NO prevents the impairment of endothelial function after menopause in females, and this improvement may result in less arterial calcification.
authors.affiliation: Institute of Health and Sports Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.
authors.forename: J-H
authors.initials: JH
authors.lastname: Park
authors.forename: M
authors.initials: M
authors.lastname: Iemitsu
authors.forename: S
authors.initials: S
authors.lastname: Maeda
authors.forename: A
authors.initials: A
authors.lastname: Kitajima
authors.forename: T
authors.initials: T
authors.lastname: Nosaka
authors.forename: N
authors.initials: N
authors.lastname: Omi
mesh_terms: D000818:Animals; D001018:Aortic Diseases / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D002114:Calcinosis / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D002118:Calcium / Q000378:metabolism; D002950:Citrate (si)-Synthase / Q000378:metabolism; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000032:analysis; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D004958:Estradiol / Q000097:blood; D005260:Female; D009043:Motor Activity / Q000502:physiology*; D018482:Muscle, Skeletal / Q000201:enzymology; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010052:Ovariectomy; D017698:Postmenopause / Q000378:metabolism / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D019332:Endothelin-1; D004958:Estradiol; D052250:Nitric Oxide Synthase Type III; D002950:Citrate (si)-Synthase; D002118:Calcium