Abstract
Male rats were treated with growth hormone (GH)-releasing hormone antiserum to induce selective GH deficiency. The chronic administration of hexarelin to these GH-deficient rats had a pronounced protective effect against ischaemic and post-ischaemic ventricular dysfunction. Hexarelin prevented hyper-responsiveness of the coronary vascular bed to angiotensin II and also prevented the reduction in generation of 6-keto-prostaglandin F1alpha in perfused hearts from GH-deficient rats. The most plausible interpretation of these findings is that hexarelin acts via stimulation of specific cardiac and vascular receptors, triggering currently unknown cytoprotective mechanisms that are responsible for resistance to ischaemic insults and for the preservation of the integrity of the endothelial vasodilation function.
MeSH terms
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6-Ketoprostaglandin F1 alpha / metabolism
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Angiotensin II / pharmacology
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Animals
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Antibodies / immunology
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Antibodies / pharmacology
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Area Under Curve
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Body Weight / drug effects
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Coronary Vessels / drug effects
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Cytoprotection / drug effects*
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / physiology
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Growth Hormone / deficiency*
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Growth Hormone / metabolism
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Growth Hormone-Releasing Hormone / antagonists & inhibitors
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Growth Hormone-Releasing Hormone / immunology
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Heart Ventricles / drug effects*
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Heart Ventricles / metabolism
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Heart Ventricles / physiopathology
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Male
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Myocardial Ischemia / drug therapy*
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Myocardial Ischemia / metabolism
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Myocardial Ischemia / physiopathology
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Myocardial Reperfusion
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Oligopeptides / administration & dosage
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Oligopeptides / pharmacology*
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Oligopeptides / therapeutic use*
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Organ Size / drug effects
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Perfusion
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Rats
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Rats, Sprague-Dawley
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Vasoconstrictor Agents / pharmacology
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Vasodilation / drug effects
Substances
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Antibodies
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Oligopeptides
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Vasoconstrictor Agents
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hexarelin
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Angiotensin II
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6-Ketoprostaglandin F1 alpha
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Growth Hormone
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Growth Hormone-Releasing Hormone