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Hypertens Res. 2019 Jun 6. doi: 10.1038/s41440-019-0273-z. [Epub ahead of print]

Renoprotective effects of voluntary running exercise training on aldosterone-induced renal injury in human L-FABP chromosomal transgenic mice.

Author information

1
Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan.
2
Faculty of Health and Sport Sciences, University of Tsukuba, Ibaraki, Japan.
3
Japan Society for the Promotion of Science, Tokyo, Japan.
4
Department of Anatomy, St. Marianna University School of Medicine, Kanagawa, Japan.
5
JCHO Tokyo Takanawa Hospital, Tokyo, Japan.
6
Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan. a2kamijo@marianna-u.ac.jp.
7
Department of Anatomy, St. Marianna University School of Medicine, Kanagawa, Japan. a2kamijo@marianna-u.ac.jp.

Abstract

Tubulointerstitial damage is a crucial therapeutic target in preventing chronic kidney disease (CKD) progression. Inappropriately activated renin-angiotensin-aldosterone system (RAAS) in the tubulointerstitial area is strongly associated with tubulointerstitial damage progression. Therefore, this study aimed to determine whether there is a beneficial effect of voluntary running exercise training on aldosterone-induced renal injury. Human L-type fatty acid-binding protein (L-FABP) chromosomal transgenic (L-FABP+/-) male mice were used to evaluate the effect of exercise by using urinary L-FABP, a tubular marker. The mice were assigned to either the exercise group that performed voluntary running exercise training using a running wheel or the control group. Subsequently, two groups were injected with aldosterone (0.125 μg kg-1 min-1) and administered 1% NaCl water, and two groups were administered aldosterone only in solvent 4 weeks after initiating the exercise. Aldosterone was injected for another 4 weeks, and NaCl water was administered from 5 weeks after starting the exercise until 8 weeks. Although both aldosterone and NaCl water significantly decreased the running distance, tubulointerstitial damage involving interstitial infiltration of macrophages and fibrosis and the elevation of urinary human L-FABP induced by aldosterone injection was prevented by voluntary running exercise training. Urinary human L-FABP levels were significantly correlated with the degree of tubulointerstitial damage. In conclusion, voluntary running exercise training delayed tubulointerstitial damage progression in the aldosterone-induced renal injury model and therefore may be a promising nonpharmacological strategy in CKD.

KEYWORDS:

Exercise training; Renin–angiotensin–aldosterone system; Tubulointerstitial damage; Urinary L-type fatty acid-binding protein

PMID:
31168059
DOI:
10.1038/s41440-019-0273-z

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