Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1994-3-8
pubmed:abstractText
Chronic hypertension is associated with impaired endothelial function [i.e., reduced synthesis/release of endothelium-derived relaxing factor (EDRF) and increased synthesis/release of endothelium-derived contracting factor (EDCF)] in both animals and humans. Although it is not known whether endothelial dysfunction is the consequence and/or an important pathogenetic cause of hypertension, the goal of effective antihypertensive therapy should include restoration of normal endothelial function as well. Because angiotensin I-converting enzyme (ACE) inhibitors are effectively used in the treatment of hypertension, the aim of the present study was to test whether in vivo treatment of spontaneously hypertensive rats (SHRs) with the ACE inhibitor cilazapril improves endothelial function in the isolated thoracic aorta of SHRs. Treatment of SHRs with cilazapril (10 mg/kg/day orally for 2 weeks) resulted in a significant decrease in blood pressure and normalization of endothelium-dependent relaxation evoked by acetylcholine (ACh) and adenosine diphosphate (ADP). However, cilazapril treatment had no significant effect on endothelium-dependent contractions evoked by 5-hydroxytryptamine (5-HT; serotonin) and prostaglandin F2 alpha (PGF2 alpha). In contrast, in vitro treatment of isolated thoracic aortas with indomethacin (10(-5) M) normalized endothelium-dependent relaxations to ACh and ADP as well as inhibited endothelium-dependent contractions to 5-HT and PGF2 alpha. These results suggest that the ACE inhibitor cilazapril increases the synthesis/release of EDRFs whereas indomethacin prevents the synthesis/release of cyclo-oxygenase-derived EDCFs in the endothelium of rat aorta. The exact mechanism of action of ACE inhibitors on endothelial dysfunction remains to be determined.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
22 Suppl 5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S23-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7508048-Acetylcholine, pubmed-meshheading:7508048-Adenosine Diphosphate, pubmed-meshheading:7508048-Animals, pubmed-meshheading:7508048-Aorta, Thoracic, pubmed-meshheading:7508048-Blood Pressure, pubmed-meshheading:7508048-Cilazapril, pubmed-meshheading:7508048-Dinoprost, pubmed-meshheading:7508048-Endothelium, Vascular, pubmed-meshheading:7508048-Hypertension, pubmed-meshheading:7508048-Indomethacin, pubmed-meshheading:7508048-Male, pubmed-meshheading:7508048-Muscle, Smooth, Vascular, pubmed-meshheading:7508048-Muscle Contraction, pubmed-meshheading:7508048-Muscle Relaxation, pubmed-meshheading:7508048-Nitroprusside, pubmed-meshheading:7508048-Phenylephrine, pubmed-meshheading:7508048-Rats, pubmed-meshheading:7508048-Rats, Inbred SHR, pubmed-meshheading:7508048-Rats, Wistar, pubmed-meshheading:7508048-Serotonin
pubmed:year
1993
pubmed:articleTitle
Effect of cilazapril and indomethacin on endothelial dysfunction in the aortas of spontaneously hypertensive rats.
pubmed:affiliation
Schering AG, Research Center, Berlin, Germany.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro