Ghrelin improves endothelial dysfunction through growth hormone-independent mechanisms in rats

Ghrelin is a novel growth hormone (GH)-releasing peptide which was isolated from the stomach. We have reported that ghrelin causes vasorelaxation in rats through GH-independent mechanisms. We investigated whether ghrelin improves endothelial dysfunction. Ghrelin was subcutaneously administered to GH...

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Published in:Biochemical and biophysical research communications Vol. 310; no. 3; pp. 830 - 835
Main Authors: Shimizu, Yoshito, Nagaya, Noritoshi, Teranishi, Yasuhiro, Imazu, Michinori, Yamamoto, Hideya, Shokawa, Tomoki, Kangawa, Kenji, Kohno, Nobuoki, Yoshizumi, Masao
Format: Journal Article
Language:English
Published: United States Elsevier Inc 24.10.2003
Subjects:
Acetylcholine - pharmacology
Animals
Aorta, Thoracic - metabolism
Arteriosclerosis - drug therapy
Blood Pressure
Blotting, Western
Body Weight
Cardiovascular Agents - pharmacology
Dose-Response Relationship, Drug
Endothelium
Endothelium, Vascular - metabolism
Enzyme Inhibitors - pharmacology
Ghrelin
Growth Hormone - metabolism
Growth substances
Heart Rate
Indomethacin - pharmacology
Male
NG-Nitroarginine Methyl Ester - pharmacology
Nitric oxide
Nitric oxide synthase
Nitric Oxide Synthase - metabolism
Nitroprusside - pharmacology
Peptide Hormones - metabolism
Peptide Hormones - pharmacology
Peptide Hormones - physiology
Placebos
Rats
Rats, Sprague-Dawley
Vasorelaxation
Nitric oxide synthase
Growth substances
Vasorelaxation
Nitric oxide
Endothelium
ISSN:0006-291X, 1090-2104
Online Access:Get full text
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Summary:Ghrelin is a novel growth hormone (GH)-releasing peptide which was isolated from the stomach. We have reported that ghrelin causes vasorelaxation in rats through GH-independent mechanisms. We investigated whether ghrelin improves endothelial dysfunction. Ghrelin was subcutaneously administered to GH-deficient rats for three weeks. After isolation of the thoracic aorta, aortic ring tension was measured to evaluate vasorelaxation. Acetylcholine-induced vasorelaxation was impaired in GH-deficient rats given placebo compared to that in normal rats given placebo. GH-deficient rats treated with ghrelin, however, showed a significant increase in the maximal relaxation as compared with those given placebo. This improvement by ghrelin was inhibited by N G-nitro- l-arginine methyl ester, a nonselective nitric oxide synthase (NOS) inhibitor. Western blot analysis demonstrated that treatment with ghrelin increased endothelial NOS (eNOS) expression in the aorta of GH-deficient rats. These results suggest that administration of ghrelin improves endothelial dysfunction and increases eNOS expression in rats through GH-independent mechanisms.
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ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2003.09.085