ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2025
Exercise pressor reflex function is augmented in rats with chronic kidney disease.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- High-Phosphate-Induced Hypertension: The Pathogenic Role of Fibroblast Growth Factor 23 (FGF23) Signaling in Sympathetic Nervous System Activation.International journal of molecular sciences · 2026Review
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8 authors.
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Abstract
Cardiovascular responses to exercise are exaggerated in patients with chronic kidney disease (CKD). Enhanced sympathetic activation is thought to play a role with the exercise pressor reflex (EPR), a reflex originating in contracting muscle, modulating this response. Previous studies suggest an overactive EPR in patients with CKD as indicated by muscle sympathetic overactivation during static handgrip exercise. However, the role of the EPR could not be fully elucidated due to experimental constraints inherent to humans. The purpose of this study was to specifically test EPR function in a CKD animal model. Male Sprague-Dawley rats were assigned to a diet containing 0.25% adenine to induce CKD or a control diet. Mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to activation of the EPR, including its functional components, the mechanoreflex and metaboreflex, were assessed in decerebrate, unanesthetized animals after feeding 10-14 wk. Plasma creatinine was significantly higher in CKD rats compared with controls (1.80 ± 0.78 vs. 0.34 ± 0.02 mg·dL
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