title: Involvement of endogenous endothelin-1 in exercise-induced redistribution of tissue blood flow: an endothelin receptor antagonist reduces the redistribution.
abstract: BACKGROUND
  Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide. Exercise results in a significant redistribution of tissue blood flow, which greatly increases blood flow in active muscles but decreases it in the splanchnic circulation. We reported that exercise causes an increase of ET-1 production in the internal organ and then hypothesized that ET-1 participates in the exercise-induced redistribution of tissue blood flow. We investigated the effects of acute endothelin-A (ETA)-receptor blockade on regional tissue blood flow during exercise in rats.
  
  
  RESULTS
  Regional blood flow in the kidney, spleen, stomach, intestine, and muscles was measured using the microsphere technique before and during treadmill running of 30 minutes duration at 30 m/min after pretreatment with either an ETA-receptor antagonist (TA-0201; 0.5 mg/kg) or vehicle in rats. Blood flow in the kidney, spleen, stomach, and intestine was decreased by exercise, but the magnitude of the decrease after pretreatment with TA-0201 was significantly smaller than that after pretreatment with vehicle. Furthermore, the increase in blood flow to active muscles induced by exercise was significantly smaller in rats pretreated with TA-0201 than those pretreated with vehicle.
  
  
  CONCLUSIONS
  The present study revealed that ET-1-mediated vasoconstriction participates in the decrease of blood flow in the internal organs of rats during exercise, and therefore, that these actions of endogenous ET-1 partly contribute to the increase of blood flow in active muscles during exercise. The data suggest that endogenous ET-1 participates in the exercise-induced redistribution of tissue blood flow.
authors.affiliation: Department of Sports Medicine, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.
authors.forename: Seiji
authors.initials: S
authors.lastname: Maeda
authors.forename: Takashi
authors.initials: T
authors.lastname: Miyauchi
authors.forename: Motoyuki
authors.initials: M
authors.lastname: Iemitsu
authors.forename: Takumi
authors.initials: T
authors.lastname: Tanabe
authors.forename: Yoko
authors.initials: Y
authors.lastname: Irukayama-Tomobe
authors.forename: Katsutoshi
authors.initials: K
authors.lastname: Goto
authors.forename: Iwao
authors.initials: I
authors.lastname: Yamaguchi
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Matsuda
mesh_terms: D000818:Animals; D001775:Blood Circulation; D004064:Digestive System / Q000098:blood supply; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects; D007189:Indans / Q000494:pharmacology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D010805:Physical Conditioning, Animal; D011743:Pyrimidines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D044022:Receptor, Endothelin A; D012039:Regional Blood Flow / Q000187:drug effects; D012079:Renal Circulation; D013152:Splanchnic Circulation; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D007189:Indans; D011743:Pyrimidines; D044022:Receptor, Endothelin A; D013449:Sulfonamides; C113972:T 0201; C087551:1H-Indene-2-carboxylic acid, 1-(1,3-benzodioxol-5-yl)-3-(2- (carboxymethoxy)-4-methoxyphenyl)-2,3-dihydro-5-propoxy-, (1S,2R,3S)-; D019344:Lactic Acid