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Related Concept Videos

Exercise and Cardiovascular Response01:20

Exercise and Cardiovascular Response

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Exercise significantly impacts cardiovascular response, which is crucial for understanding patient health and designing effective treatment plans.
Light to moderate physical activity initiates a series of interconnected responses in the body. The heart rate modestly increases in anticipation of the workout, followed by widespread vasodilation as oxygen consumption by skeletal muscles increases. This results in decreased peripheral resistance, increased capillary blood flow, and accelerated...
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Related Experiment Video

Updated: May 29, 2025

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PAG Masked Protective Physical Exercise-Induced High H2S Levels in 5/6 Nephrectomized Rats.

Behjat Seifi1, Mehri Kadkhodaei1, Enayatollah Bakhshi2

  • 1Department of Physiology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Iranian Journal of Pharmaceutical Research : IJPR
|February 3, 2025
PubMed
Summary

Exercise benefits in chronic kidney disease (CKD) may involve hydrogen sulfide (H2S) signaling. Inhibiting H2S production with D, L-propargylglycine (PAG) reversed exercise-induced improvements in CKD rats.

Keywords:
5/6 NephrectomyExerciseHydrogen SulfideHypertensionPAGRSNA

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Area of Science:

  • Nephrology
  • Exercise Physiology
  • Biochemistry

Background:

  • Chronic kidney disease (CKD) is a global health concern.
  • Exercise is a potential therapeutic intervention for CKD.
  • Mechanisms underlying exercise benefits in CKD require elucidation.

Purpose of the Study:

  • To investigate the role of hydrogen sulfide (H2S) in mediating the protective effects of exercise in a preclinical model of CKD.
  • To examine how inhibiting H2S production affects oxidative stress and inflammation markers during exercise in CKD.

Main Methods:

  • Male Wistar rats underwent 5/6 nephrectomy to induce CKD.
  • Rats were subjected to 8 weeks of exercise training.
  • D, L-propargylglycine (PAG), a cystathionine γ-lyase (CSE) inhibitor, was administered to block H2S production.
  • Systolic blood pressure (BP), renal sympathetic nerve activity (RSNA), creatinine, BUN, oxidative stress, and inflammatory markers were assessed.

Main Results:

  • PAG administration reversed exercise-induced improvements in kidney function markers (creatinine, BUN).
  • Inhibition of H2S production by PAG negated exercise-induced reductions in oxidative stress (MDA, SOD) and inflammation (TNF-α, IL-6).
  • PAG treatment also reversed exercise-induced decreases in elevated RSNA and BP in CKD rats.

Conclusions:

  • Exercise-mediated improvements in blood pressure, oxidative stress, and inflammation in CKD may be partly attributed to the CSE/H2S signaling pathway.
  • H2S plays a significant role in the renoprotective effects of physical activity in CKD.
  • Targeting the H2S pathway could be a potential therapeutic strategy for managing CKD.