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Exercise training enhances flow-mediated dilation in spontaneously hypertensive rats.

F Gündüz1, G Koçer, S Ulker

  • 1Akdeniz University, Medical Faculty, Department of Physiology, Antalya, Turkey. fgunduz@akdeniz.edu.tr

Physiological Research
|May 18, 2011
PubMed
Summary

Exercise training improves blood vessel function in spontaneously hypertensive rats. This enhancement in flow-mediated dilation (FMD) is primarily mediated by endothelium-derived hyperpolarizing factors (EDHF).

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Area of Science:

  • Cardiovascular Physiology
  • Exercise Science
  • Vascular Biology

Background:

  • Spontaneously hypertensive rats (SHR) exhibit impaired vascular function, including reduced flow-mediated dilation (FMD).
  • Exercise training is a known intervention to improve cardiovascular health, but its specific effects on FMD in SHR require detailed investigation.

Purpose of the Study:

  • To investigate the impact of exercise training on FMD in gastrocnemius muscle arteries of SHR.
  • To elucidate the specific vasoactive mechanisms (nitric oxide, prostaglandins, EDHF) underlying exercise-induced improvements in FMD in SHR.

Main Methods:

  • SHR and WKY rats were subjected to an eight-week swimming exercise program or remained sedentary.
  • Flow-mediated dilation (FMD) of isolated gastrocnemius arteries was assessed using a pressurized myograph.
  • Pharmacological antagonists (L-NAME, indomethacin, TEA) were used to inhibit nitric oxide synthase, cyclooxygenase, and EDHF pathways, respectively.

Main Results:

  • FMD was significantly blunted in arteries from sedentary SHR compared to WKY rats.
  • Exercise training significantly improved FMD in SHR arteries.
  • In trained SHR, the enhanced FMD was primarily mediated by endothelium-derived hyperpolarizing factors (EDHF), with nitric oxide and prostaglandins playing lesser roles.

Conclusions:

  • Exercise training effectively improves flow-mediated dilation in spontaneously hypertensive rats.
  • The beneficial effects of exercise training on vascular function in SHR are predominantly mediated through EDHF-dependent pathways.