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Related Experiment Video

Updated: May 26, 2025

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

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Exercise pressor reflex function is augmented in rats with chronic kidney disease.

Han-Kyul Kim^1,2, Juan A Estrada², Ayumi Fukazawa²

¹Department of Internal Medicine-Cardiology Division, UT Southwestern Medical Center, Dallas, Texas, United States.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology

|February 25, 2025

Summary

The exercise pressor reflex (EPR) is exaggerated in chronic kidney disease (CKD). This heightened response involves sympathetic overactivation and augmented mechanoreflex and metaboreflex function in CKD.

Keywords:

blood pressure chronic kidney disease exercise pressor reflex sympathetic nerve activity

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Area of Science:

Physiology
Nephrology
Cardiovascular Science

Background:

Cardiovascular responses to exercise are often exaggerated in patients with chronic kidney disease (CKD).
Enhanced sympathetic activation, potentially mediated by the exercise pressor reflex (EPR) originating in contracting muscles, is implicated in this phenomenon.
Previous human studies suggest an overactive EPR in CKD, but experimental limitations hinder full elucidation.

Purpose of the Study:

To specifically test the function of the exercise pressor reflex (EPR) in a validated animal model of chronic kidney disease (CKD).

Main Methods:

Male Sprague-Dawley rats were fed a diet containing 0.25% adenine to induce CKD or a control diet.
In decerebrate, unanesthetized animals, mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to EPR activation were assessed.
Functional components of the EPR, including the mechanoreflex (passive muscle stretch) and metaboreflex (intra-arterial capsaicin), were evaluated.

Main Results:

CKD rats exhibited significantly higher plasma creatinine levels compared to controls.
Both MAP and RSNA responses to muscle contraction (EPR activation) were potentiated in CKD rats.
Responses to passive muscle stretch (mechanoreflex) and intra-arterial capsaicin (metaboreflex) were also significantly augmented in CKD animals.

Conclusions:

The exercise pressor reflex (EPR), including its mechanoreflex and metaboreflex components, is exaggerated in a rat model of chronic kidney disease (CKD).
This exaggerated EPR contributes to heightened pressor responses and sympathetic overactivation during muscle contraction in CKD.
Findings suggest augmented EPR, mechanoreflex, and metaboreflex function in the context of CKD.