Linked Life Data

10471007

Source:http://linkedlifedata.com/resource/pubmed/id/10471007

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-10-22
pubmed:abstractText
The endothelial vasodilation mechanism(s) has been investigated in aortic rings of hypophysectomized male rats as well as hypophysectomized rats treated for 7 days with growth hormone (GH, 400 microg/kg, s.c.) or hexarelin (80 microg/kg, s.c.). Tissue preparations from intact animals were taken as controls. The results obtained indicate that the release of 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) from aortic rings of hypophysectomized rats was markedly reduced (51%; p<0.01) as compared with that of control preparations; the peak response to cumulative concentration of endothelin-1 (ET-1, from 10(-11) to 10(-5) M) was increased 2.4-fold (p<0.01) versus controls; the relaxant activity of acetylcholine (ACh, from 10(-10) to 10(-4) M) in norepinephrine-precontracted aortic rings was reduced by 39.5+/-4.4%. Pretreatment of hypophysectomized rats with GH or hexarelin markedly antagonized the hyperresponsiveness of the aortic tissue to ET-1 and allowed a consistent recovery of both the relaxant activity of ACh and the generation of 6-keto-PGF1alpha. Collectively these findings support the concept that dysfunction of vascular endothelial cells may be induced by a defective GH function. Because a replacement regimen of GH restored the somatotropic function and increased plasma insulin-like growth factor-I (IGF-I) concentrations in the hypophysectomized rats, it is suggested that IGF-I may have protected the vascular endothelium acting as a biologic mediator of GH action. In contrast to GH, hexarelin replacement neither increased body weight nor affected the plasma concentrations of IGF-I, indicating that its beneficial action on vascular endothelium was divorced from that on somatotropic function and was likely due to activation of specific endothelial receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
454-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10471007-6-Ketoprostaglandin F1 alpha, pubmed-meshheading:10471007-Acetylcholine, pubmed-meshheading:10471007-Animals, pubmed-meshheading:10471007-Aorta, pubmed-meshheading:10471007-Body Weight, pubmed-meshheading:10471007-Endothelin-1, pubmed-meshheading:10471007-Endothelium, Vascular, pubmed-meshheading:10471007-Enzyme Inhibitors, pubmed-meshheading:10471007-Homeostasis, pubmed-meshheading:10471007-Human Growth Hormone, pubmed-meshheading:10471007-Humans, pubmed-meshheading:10471007-Hypophysectomy, pubmed-meshheading:10471007-Male, pubmed-meshheading:10471007-Oligopeptides, pubmed-meshheading:10471007-Protective Agents, pubmed-meshheading:10471007-Rats, pubmed-meshheading:10471007-Rats, Sprague-Dawley, pubmed-meshheading:10471007-Vasodilation, pubmed-meshheading:10471007-omega-N-Methylarginine
pubmed:year
1999
pubmed:articleTitle
Growth hormone and hexarelin prevent endothelial vasodilator dysfunction in aortic rings of the hypophysectomized rat.
pubmed:affiliation
Department of Pharmacology, Chemotherapy and Medical Toxicology, University of Milan, Italy. giuseppe.rossoni@unimi.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't