Linked Life Data

9622146

Source:http://linkedlifedata.com/resource/pubmed/id/9622146

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-6-19
pubmed:abstractText
Endothelin partially mediates angiotensin (Ang) II-induced vascular changes in vivo. This study investigated the effects of the angiotensin type 1 receptor antagonist losartan and the calcium channel blocker verapamil on vascular reactivity and tissue endothelin-1 levels in aortas of Wistar-Kyoto rats treated for 2 weeks with Ang II (200 ng x kg(-1) x min(-1)). Ang II increased systolic blood pressure (39+/-4 mm Hg, P<0.05). Concomitant treatment with losartan abolished the Ang II-induced pressure increase (P<0.05), whereas verapamil reduced it only partially (P<0.05). In the aortas of rats with Ang II-induced hypertension, tissue endothelin-1 content was increased threefold and contractions to endothelin-1 were impaired (P<0.05). Interestingly, these alterations were normalized by losartan (P<0.05) but not by verapamil. Hence, there was a strong, negative correlation between contractions to endothelin-1 and tissue endothelin-1 content (r=-0.733, P<0.0001). In contrast, both antihypertensive drugs normalized impaired endothelium-dependent relaxations to acetylcholine and reduced the sensitivity of vascular smooth muscle to sodium nitroprusside compared with Ang II-treated rats (P<0.05). Ang II-induced hypertension enhanced endothelium-dependent contractions to acetylcholine, and these were normalized by either drug. In conclusion, these findings suggest that long-term treatment with Ang II modulates endothelin-1 protein expression in the rat aorta. Although both antihypertensive agents lowered blood pressure and normalized endothelial function, only losartan prevented the increase in tissue endothelin-1 content, suggesting that angiotensin type 1 receptor antagonists but not calcium antagonists modulate tissue endothelin-1 in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1305-10
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9622146-Angiotensin II, pubmed-meshheading:9622146-Animals, pubmed-meshheading:9622146-Antihypertensive Agents, pubmed-meshheading:9622146-Aorta, Thoracic, pubmed-meshheading:9622146-Blood Pressure, pubmed-meshheading:9622146-Calcium Channel Blockers, pubmed-meshheading:9622146-Data Interpretation, Statistical, pubmed-meshheading:9622146-Endothelin-1, pubmed-meshheading:9622146-Endothelium, Vascular, pubmed-meshheading:9622146-Hypertension, pubmed-meshheading:9622146-Losartan, pubmed-meshheading:9622146-Male, pubmed-meshheading:9622146-Muscle, Smooth, Vascular, pubmed-meshheading:9622146-Nitroprusside, pubmed-meshheading:9622146-Rats, pubmed-meshheading:9622146-Rats, Inbred WKY, pubmed-meshheading:9622146-Receptors, Endothelin, pubmed-meshheading:9622146-Time Factors, pubmed-meshheading:9622146-Vasoconstriction, pubmed-meshheading:9622146-Vasodilation, pubmed-meshheading:9622146-Vasodilator Agents, pubmed-meshheading:9622146-Verapamil
pubmed:year
1998
pubmed:articleTitle
Losartan but not verapamil inhibits angiotensin II-induced tissue endothelin-1 increase: role of blood pressure and endothelial function.
pubmed:affiliation
Cardiovascular Research, Institute of Physiology, University of Zürich, University Hospital, Zürich, Switzerland.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't