on October 7, 2002
Published online before print October 7, 2002, doi: 10.1161/01.CIR.0000038362.16740.A2
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Submitted on June 20, 2002
From the Department of Sports Medicine, Institute of Health and Sport Sciences (S.M., T.T., Y.I.-T., M.M.), Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine (T.M., M.I., I.Y.), and Department of Pharmacology (K.G.), University of Tsukuba, Tsukuba, Ibaraki, Japan. * To whom correspondence should be addressed. E-mail: m-matsuda{at}taiiku.tsukuba.ac.jp.
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. Methods and 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.
Revised on August 19, 2002
Accepted on August 30, 2002
Involvement of Endogenous Endothelin-1 in Exercise-Induced Redistribution of Tissue Blood Flow. An Endothelin Receptor Antagonist Reduces the Redistribution
Seiji Maeda PhD,
Key words: endothelin • exercise • blood flow • receptors
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