title: Acute exercise causes an enhancement of tissue renin-angiotensin system in the kidney in rats.
abstract: OBJECTIVE
  Initially, the renin-angiotensin system (RAS) produced through the classical endocrine pathway was well known for its regulation of blood pressure. However, it was revealed that a local autocrine and/or paracrine RAS may exist in a number of tissues (such as kidney). Exercise causes a redistribution of tissue blood flow, by which the blood flow is greatly increased in active muscles, whereas it is decreased in the splanchnic circulation (such as in the kidney). We hypothesized that exercise causes an enhancement of tissue RAS in the kidney.
  
  
  METHODS
  We studied whether exercise affects expression of angiotensinogen and angiotensin-converting enzyme (ACE) and tissue angiotensin II level in the kidney. The rats performed treadmill running for 30-min. Immediately after this exercise, kidney was quickly removed. Control rats remained at rest during this 30-min period.
  
  
  RESULTS
  The expression of angiotensinogen mRNA in the kidney was markedly higher in the exercise rats than in the control rats. ACE mRNA in the kidney was significantly higher in the exercise rats than in the control rats. Western blot analysis confirmed significant upregulation of ACE protein in the kidney after exercise. Tissue angiotensin II level was also increased by exercise.
  
  
  CONCLUSIONS
  The present study suggests that the exercise-induced enhancement of tissue RAS in the kidney causes vasoconstriction and hence decreases blood flow in the kidney, which are helpful in increasing blood flow in active muscles, thereby contributing to the redistribution of blood flow during exercise.
authors.affiliation: Center for Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Ibaraki, Japan. smaeda@tara.tsukuba.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Maeda
authors.forename: M
authors.initials: M
authors.lastname: Iemitsu
authors.forename: S
authors.initials: S
authors.lastname: Jesmin
authors.forename: T
authors.initials: T
authors.lastname: Miyauchi
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000808:Angiotensinogen / Q000096:biosynthesis / Q000235:genetics; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D015153:Blotting, Western; D005786:Gene Expression Regulation; D007668:Kidney / Q000098:blood supply / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D007703:Peptidyl-Dipeptidase A / Q000096:biosynthesis / Q000235:genetics; D005082:Physical Exertion / Q000502:physiology*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System / Q000502:physiology*; D013154:Spleen / Q000098:blood supply
chemical_list: D012333:RNA, Messenger; D000808:Angiotensinogen; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A