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<p>Arterial hypertension leads to urological complications by impairing urinary bladder function. Physical exercise, particularly high-intensity interval training (HIIT), is a non-pharmacological strategy for blood pressure control. HIIT improves oxygen consumption, body composition, and cardiovascular health, but its effects on the urinary bladder remain unclear. This study evaluated the effects of HIIT on structural and molecular markers of urinary bladder remodeling in spontaneously hypertensive rats (SHR), with emphasis on fibrosis, neurotrophic and angiogenic signaling, hypoxia-related pathways, and the balance between the ACE/Ang II/AT1R and ACE2/Ang-(1-7)/MasR axes. We also assessed its effects on blood pressure, metabolism, and redox biomarkers in blood circulation. HIIT significantly reduced serum glucose and lipid levels while improving redox balance with increased antioxidants. In the bladder, HIIT downregulated VEGF and NGF, reduced collagen deposition, and decreased TGF-β and SMAD2 expression. Additionally, HIIT modulated the angiotensin receptor axis (AT1/MAS ratio) and upregulated VEGF, promoting angiogenesis. Publicly available microarray data from ischemic and aging models support our findings, highlighting the role of TGF-β pathways in bladder fibrosis. This study reveals key intracellular mechanisms linking HIIT to redox balance, fibrosis, hypoxia, vascular remodeling, and angiotensin receptor modulation. Together, our findings suggest HIIT as a potential therapeutic approach for vascular and structural remodeling in the hypertensive urinary bladder.</p><p></p>

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High-intensity interval training attenuates urothelial nerve growth factor and angiotensin axis in hypertensive urinary bladder

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月20日

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  • Victor Rogério Garcia Batista,
  • Maria Eduarda Almeida Tavares,
  • Ivo Vieira de Sousa Neto,
  • Rafael Jesus Gonçalves Rubira,
  • Tatiana Aparecida de Oliveira,
  • Allice Santos Cruz Veras,
  • Antonio Hernandes Chaves-Neto,
  • Francilene Lima Agostinho de Souza,
  • Francis Lopes Pacagnelli,
  • Vítor Samuel Leite Fernandes,
  • Giovana Rampazzo Teixeira

摘要

Arterial hypertension leads to urological complications by impairing urinary bladder function. Physical exercise, particularly high-intensity interval training (HIIT), is a non-pharmacological strategy for blood pressure control. HIIT improves oxygen consumption, body composition, and cardiovascular health, but its effects on the urinary bladder remain unclear. This study evaluated the effects of HIIT on structural and molecular markers of urinary bladder remodeling in spontaneously hypertensive rats (SHR), with emphasis on fibrosis, neurotrophic and angiogenic signaling, hypoxia-related pathways, and the balance between the ACE/Ang II/AT1R and ACE2/Ang-(1-7)/MasR axes. We also assessed its effects on blood pressure, metabolism, and redox biomarkers in blood circulation. HIIT significantly reduced serum glucose and lipid levels while improving redox balance with increased antioxidants. In the bladder, HIIT downregulated VEGF and NGF, reduced collagen deposition, and decreased TGF-β and SMAD2 expression. Additionally, HIIT modulated the angiotensin receptor axis (AT1/MAS ratio) and upregulated VEGF, promoting angiogenesis. Publicly available microarray data from ischemic and aging models support our findings, highlighting the role of TGF-β pathways in bladder fibrosis. This study reveals key intracellular mechanisms linking HIIT to redox balance, fibrosis, hypoxia, vascular remodeling, and angiotensin receptor modulation. Together, our findings suggest HIIT as a potential therapeutic approach for vascular and structural remodeling in the hypertensive urinary bladder.