Endurance exercise training improves endothelium-dependent relaxation in brachial arteries from hypercholesterolemic male pigs

Department of Biomedical Sciences, University of Missouri, Columbia, Missouri Submitted 16 March 2005 ; accepted in final form 17 June 2005 We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (B...

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Published inJournal of applied physiology (1985) Vol. 99; no. 4; pp. 1412 - 1421
Main Authors Woodman, Christopher R, Thompson, Mark A, Turk, James R, Laughlin, M. Harold
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Published Bethesda, MD Am Physiological Soc 01.10.2005
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Abstract Department of Biomedical Sciences, University of Missouri, Columbia, Missouri Submitted 16 March 2005 ; accepted in final form 17 June 2005 We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1 ) NF-Sed, 2 ) NF-Ex, 3 ) HF-Sed, and 4 ) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of N G -nitro- L -arginine methyl ester ( L -NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or L -NAME + Indo. ACh- and BK-induced relaxation was inhibited by L -NAME, and L -NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of L -NAME or L -NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin. nitric oxide; prostacyclin; endothelium-derived hyperpolarizing factor; endothelial nitric oxide synthase; vascular smooth muscle Address for reprint requests and other correspondence: C. R. Woodman, Dept. of Biomedical Sciences, W108 Veterinary Medicine, 1600 E. Rollins Rd., Univ. of Missouri, Columbia, MO 65211 (e-mail: woodmanc{at}missouri.edu )
AbstractList We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1) NF-Sed, 2) NF-Ex, 3) HF-Sed, and 4) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of N(G)-nitro-l-arginine methyl ester (l-NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or l-NAME + Indo. ACh- and BK-induced relaxation was inhibited by l-NAME, and l-NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of l-NAME or l-NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin.
We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1) NF-Sed, 2) NF-Ex, 3) HF-Sed, and 4) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of NG-nitro-L-arginine methyl ester (L-NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or L-NAME + Indo. ACh- and BK-induced relaxation was inhibited by L-NAME, and L-NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of L-NAME or L-NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin. [PUBLICATION ABSTRACT]
Department of Biomedical Sciences, University of Missouri, Columbia, Missouri Submitted 16 March 2005 ; accepted in final form 17 June 2005 We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1 ) NF-Sed, 2 ) NF-Ex, 3 ) HF-Sed, and 4 ) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of N G -nitro- L -arginine methyl ester ( L -NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or L -NAME + Indo. ACh- and BK-induced relaxation was inhibited by L -NAME, and L -NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of L -NAME or L -NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin. nitric oxide; prostacyclin; endothelium-derived hyperpolarizing factor; endothelial nitric oxide synthase; vascular smooth muscle Address for reprint requests and other correspondence: C. R. Woodman, Dept. of Biomedical Sciences, W108 Veterinary Medicine, 1600 E. Rollins Rd., Univ. of Missouri, Columbia, MO 65211 (e-mail: woodmanc{at}missouri.edu )
We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1) NF-Sed, 2) NF-Ex, 3) HF-Sed, and 4) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of N G -nitro-l-arginine methyl ester (l-NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or l-NAME + Indo. ACh- and BK-induced relaxation was inhibited by l-NAME, and l-NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of l-NAME or l-NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin.
We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1) NF-Sed, 2) NF-Ex, 3) HF-Sed, and 4) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of N super(G)-nitro-L-arginine methyl ester (L-NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or L-NAME + Indo. ACh- and BK-induced relaxation was inhibited by L-NAME, and L-NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of L-NAME or L-NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin.
Author Thompson, Mark A
Woodman, Christopher R
Turk, James R
Laughlin, M. Harold
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Issue 4
Keywords Physical exercise
endothelium-derived hyperpolarizing factor: endothelial nitric oxide synthase
Physical training
Prostaglandin I2
Lipids
Smooth muscle
Male
Hyperlipoproteinemia
Lipoprotein
Relaxation
Endurance
Dyslipemia
Ungulata
vascular smooth muscle
Enzyme
prostacyclin
Brachial artery
Metabolic diseases
Cholesterol
Nitric-oxide synthase
Endothelium
Pig
Vertebrata
Mammalia
Hypercholesterolemia
Nitric oxide
Artiodactyla
Oxidoreductases
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Snippet Department of Biomedical Sciences, University of Missouri, Columbia, Missouri Submitted 16 March 2005 ; accepted in final form 17 June 2005 We tested the...
We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial...
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SubjectTerms Acetylcholine - pharmacology
Animals
Biological and medical sciences
Blood vessels
Brachial Artery - drug effects
Brachial Artery - metabolism
Brachial Artery - physiopathology
Bradykinin - pharmacology
Caveolin 1 - metabolism
Endothelium, Vascular - physiopathology
Exercise
Fundamental and applied biological sciences. Psychology
Hogs
Hypercholesterolemia - physiopathology
Immunoblotting
Immunohistochemistry
In Vitro Techniques
Male
Nitric oxide
Nitric Oxide Synthase Type III - metabolism
Nitroprusside - pharmacology
Physical Conditioning, Animal
Physical Endurance
Superoxide Dismutase - metabolism
Superoxide Dismutase-1
Swine
Swine, Miniature
Vasodilation
Vasodilator Agents - pharmacology
Title Endurance exercise training improves endothelium-dependent relaxation in brachial arteries from hypercholesterolemic male pigs
URI http://jap.physiology.org/cgi/content/abstract/99/4/1412
https://www.ncbi.nlm.nih.gov/pubmed/15976363
https://www.proquest.com/docview/222182049
https://search.proquest.com/docview/17666948
https://search.proquest.com/docview/68581675
Volume 99
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