Journal
MEDICINE & SCIENCE IN SPORTS & EXERCISE
Volume 54, Issue 7, Pages 1105-1113Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0000000000002901
Keywords
SALT-SENSITIVE HYPERTENSION; GLOMERULAR INJURY; RENAL PROTECTION; ANGIOTENSIN-CONVERTING ENZYME; ANGIOTENSINOGEN; ANGIOTENSIN II
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Funding
- JSPS KAKENHI grant [15K01360, 17H02119, 19K19888, 20H04054]
- Grants-in-Aid for Scientific Research [20H04054, 17H02119, 15K01360, 19K19888] Funding Source: KAKEN
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Exercise training can alleviate renal dysfunction, glomerular injury, and renal RAS dysregulation caused by a high-salt diet in Dahl salt-sensitive rats.
Purpose Exercise training (Ex) has antihypertensive and renal protective effects; however, the precise mechanisms remain unclear. The renal renin-angiotensin system (RAS) plays a vital role in renal function and pathology. Therefore, we investigated the effects of Ex on the renal RAS components in Dahl salt-sensitive (Dahl-S) rats. Methods Male Dahl-S rats were divided into four groups: normal salt diet + sedentary, normal salt diet + Ex, high-salt diet (HS, 8% NaCl) + sedentary, and HS + Ex. Treadmill running was performed for 8 wk in the Ex groups. Results Ex attenuated the HS-induced renal dysfunction and glomerular injury without causing blood pressure alterations. HS increased urinary excretion of both total and intact angiotensinogen. Ex decreased the HS-induced increased urinary excretion of total angiotensinogen. However, it did not change the HS-induced urinary excretion of intact angiotensinogen, indicating reduced intact angiotensinogen cleaving. Ex restored the HS-induced increased angiotensinogen and angiotensin II type 1 receptor expressions in the outer medulla and the HS-induced increased angiotensin-converting enzyme expression in the cortex. Ex restored the HS-induced decreased renin expression in the cortex and outer medulla, and the HS-induced decreased angiotensin-converting enzyme 2, angiotensin II type 2 receptor, and Mas receptor expressions in the outer medulla. Conclusions Ex attenuates HS-induced renal dysfunction, glomerular injury, and renal RAS dysregulation in Dahl-S rats.
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