Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1995-2-8
|
| pubmed:abstractText |
The role of endothelium in angiotensin II-induced contractions of the rabbit aorta and the mechanism involved were investigated. Destruction of the endothelium significantly shifted the concentration-response curve for angiotensin II to the left in a non-parallel manner and enhanced the maximal response. The EC50 and Emax values obtained from the rings with and without functional endothelium were 2.44 +/- 0.13 x 10(-9) M, 4.50 +/- 0.45 g and 1.21 +/- 0.14 x 10(-9) M (n = 8, P < 0.05), 5.73 +/- 0.55 g (n = 8, P < 0.05), respectively. Indomethacin (10(-5) M) did not significantly alter the concentration-dependent response to angiotensin II in the presence of endothelium. Three inhibitors of nitric oxide synthase (NG-monomethyl-L-arginine; NG-nitro-L-arginine, and NG-nitro-L-arginine methyl ester) at 10(-4) M caused a similar endothelium-dependent potentiation of angiotensin II-induced contractions in the aortic rings with, but not in those without endothelium. These effects were reversed by L-arginine (3 x 10(-3) M) but not by D-arginine (3 x 10(-3) M). Angiotensin II in a concentration range of 10(-16) to 10(-6) M did not relax the endothelium-intact rings precontracted with phenylephrine (2 x 10(-7) M). In the presence of endothelium, the angiotensin II subtype 2 receptor antagonist, 1-[(4-amino-3-methylphenyl]-5-(diphenylacetyl)-4,5,6,7-tetrahydro- 1H- imidazol[4,5-C]pyridine-6-carboxylic acid (PD 123177), caused neither relaxation of the rings precontracted with phenylephrine nor alteration of the concentration-response curve for angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Indomethacin,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroarginine,
http://linkedlifedata.com/resource/pubmed/chemical/PD 123177,
http://linkedlifedata.com/resource/pubmed/chemical/Pyridines,
http://linkedlifedata.com/resource/pubmed/chemical/omega-N-Methylarginine
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
|
| pubmed:issn |
0014-2999
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
12
|
| pubmed:volume |
262
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
247-53
|
| pubmed:dateRevised |
2010-11-18
|
| pubmed:meshHeading |
pubmed-meshheading:7813589-Acetylcholine,
pubmed-meshheading:7813589-Angiotensin II,
pubmed-meshheading:7813589-Angiotensin Receptor Antagonists,
pubmed-meshheading:7813589-Animals,
pubmed-meshheading:7813589-Aorta,
pubmed-meshheading:7813589-Arginine,
pubmed-meshheading:7813589-Dose-Response Relationship, Drug,
pubmed-meshheading:7813589-Endothelium, Vascular,
pubmed-meshheading:7813589-Imidazoles,
pubmed-meshheading:7813589-Indomethacin,
pubmed-meshheading:7813589-Male,
pubmed-meshheading:7813589-Muscle, Smooth, Vascular,
pubmed-meshheading:7813589-Muscle Contraction,
pubmed-meshheading:7813589-Muscle Relaxation,
pubmed-meshheading:7813589-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:7813589-Nitric Oxide,
pubmed-meshheading:7813589-Nitroarginine,
pubmed-meshheading:7813589-Pyridines,
pubmed-meshheading:7813589-Rabbits,
pubmed-meshheading:7813589-omega-N-Methylarginine
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Endothelium-dependent, nitric oxide-mediated inhibition of angiotensin II-induced contractions in rabbit aorta.
|
| pubmed:affiliation |
Department of Pharmacotherapy, University of Amsterdam, Netherlands.
|
| pubmed:publicationType |
Journal Article,
In Vitro
|