Molecular and Cellular Biochemistry

, Volume 375, Issue 1–2, pp 199–206 | Cite as

Contribution of hydrogen sulfide and nitric oxide to exercise-induced attenuation of aortic remodeling and improvement of endothelial function in spontaneously hypertensive rats

  • Qi GuEmail author
  • Bing Wang
  • Xiao-Feng Zhang
  • Yan-Ping Ma
  • Jian-Dong Liu
  • Xiao-Ze Wang


It is well known that exercise training attenuates aortic remodeling and improves endothelial function in spontaneously hypertensive rats (SHR). However, the underlying molecular mechanism remains unclear. Hydrogen sulfide (H2S) and nitric oxide (NO), as two established physiologic messenger molecules, have important roles in the development of aortic remodeling and endothelial dysfunction in hypertensive animals and patients. In this work, it was found that exercise training had no significant effect on blood pressure, but effectively attenuated baroreflex dysfunction in SHR. Exercise training in SHR attenuated aortic remodeling and improved endothelium-mediated vascular relaxations of aortas in response to acetylcholine. Interestingly, exercise training in SHR restored plasma H2S levels and aortic H2S formation and enhanced levels of mRNA for cystathionine γ-lyase in aortas. Furthermore, exercise training in SHR resulted in augmentation of nitrite and nitrate (NOx) contents and reduction of asymmetric dimethylarginine contents of aortas, upregulation of dimethylarginine dimethylaminohydrolase 2, and phosphorylation of nitric oxide synthase 3, but had no significant effect on protein levels of NOS3. In addition, exercise training could effectively reduce malondialdehyde production and suppressed formation of O2 , and OONO in aortas of SHR through enhancing activities of superoxide dismutase and catalase, and suppressing NADPH oxidase activity. In conclusion, exercise training ameliorates aortic hypertrophy and endothelial dysfunction, possibly via restoring bioavailabilities of hydrogen sulfide and nitric oxide in SHR.


Exercise training Spontaneously hypertensive rats Aortic remodeling Endothelial dysfunction Hydrogen sulfide Nitric oxide 


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Copyright information

© Springer Science+Business Media New York 2012

Authors and Affiliations

  • Qi Gu
    • 1
    Email author
  • Bing Wang
    • 1
  • Xiao-Feng Zhang
    • 2
  • Yan-Ping Ma
    • 3
  • Jian-Dong Liu
    • 4
  • Xiao-Ze Wang
    • 5
  1. 1.School of Physical Education Xi’an Technological UniversityXi’anChina
  2. 2.Department of GynecologyChengyang People’s HospitalQingdaoChina
  3. 3.Department of NeurologyChengyang People’s HospitalQingdaoChina
  4. 4.Department of GastroenterologyThe Third People’s Hospital of DatongDatongChina
  5. 5.Department of General SurgeryYuquan Hospital of Tsinghua UniversityBeijingChina

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