論文

査読有り 最終著者 国際誌
2022年7月

Effects of Exercise Training on the Renin–Angiotensin System in the Kidneys of Dahl Salt-Sensitive Rats

Medicine & Science in Sports & Exercise
  • Akihiro Sakuyama
  • ,
  • Yoshiko Ogawa
  • ,
  • Lusi Xu
  • ,
  • Miwa Komatsu
  • ,
  • Takahiro Miura
  • ,
  • Asako Namai-Takahash
  • ,
  • Masahiro Kohzuki
  • ,
  • Osamu Ito

54
7
開始ページ
1105
終了ページ
1113
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1249/mss.0000000000002901
出版者・発行元
Ovid Technologies (Wolters Kluwer Health)

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 eight weeks 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.

リンク情報
DOI
https://doi.org/10.1249/mss.0000000000002901
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/35220367
URL
https://journals.lww.com/10.1249/MSS.0000000000002901
ID情報
  • DOI : 10.1249/mss.0000000000002901
  • ISSN : 0195-9131
  • eISSN : 1530-0315
  • PubMed ID : 35220367

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