rdf:type |
|
lifeskim:mentions |
umls-concept:C0003015,
umls-concept:C0006100,
umls-concept:C0006104,
umls-concept:C0006675,
umls-concept:C0028128,
umls-concept:C0033567,
umls-concept:C0072970,
umls-concept:C1135183,
umls-concept:C1180238,
umls-concept:C1383501,
umls-concept:C1627358,
umls-concept:C2349975
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pubmed:issue |
1-2
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pubmed:dateCreated |
1994-7-7
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pubmed:abstractText |
We studied whether primary cultured porcine brain capillary endothelial cells (PBCEC) respond to bradykinin with an enhanced intracellular cytosolic calcium concentration [Ca2+]i with subsequent formation of nitric oxide (NO) and prostacyclin (PGI2). In addition we examined whether these cells synthetize and release kinins that may accumulate during angiotensin-converting enzyme (ACE) inhibition. [Ca2+]i was assessed by the fluorescent dye Fura-2, NO formation by determination of intracellular cyclic GMP and PGI2 by a specific radioimmunoassay for 6-ketoprostaglandin F1 alpha. Bradykinin and the ACE inhibitor ramiprilat concentration-dependently increased the formation of cyclic GMP which was completely prevented by the stereospecific inhibitor of NO synthase, NG-nitro-L-arginine. Also the specific B2-kinin receptor antagonist icatibant (Hoe 140) abolished the increase in cyclic GMP as well as the ramiprilat-induced increase in PGI2 formation. The data demonstrate the existence of B2-kinin receptors and ACE activity in PBCEC. Moreover PBCEC are capable of producing and releasing kinins in amounts that lead via stimulation of B2-kinin receptors to an enhanced [Ca2+]i as well as NO and PGI2 synthesis and release, provided that degradation of kinins is prevented by inhibition of endothelial ACE activity.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-Methyl-3-isobutylxanthine,
http://linkedlifedata.com/resource/pubmed/chemical/6-Ketoprostaglandin F1 alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/Bradykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Epoprostenol,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroarginine,
http://linkedlifedata.com/resource/pubmed/chemical/Ramipril,
http://linkedlifedata.com/resource/pubmed/chemical/ramiprilat
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
|
pubmed:issn |
0006-8993
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
28
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pubmed:volume |
638
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
261-6
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:7515323-1-Methyl-3-isobutylxanthine,
pubmed-meshheading:7515323-6-Ketoprostaglandin F1 alpha,
pubmed-meshheading:7515323-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:7515323-Animals,
pubmed-meshheading:7515323-Arginine,
pubmed-meshheading:7515323-Bradykinin,
pubmed-meshheading:7515323-Calcium,
pubmed-meshheading:7515323-Capillaries,
pubmed-meshheading:7515323-Cells, Cultured,
pubmed-meshheading:7515323-Cerebrovascular Circulation,
pubmed-meshheading:7515323-Cyclic GMP,
pubmed-meshheading:7515323-Cytosol,
pubmed-meshheading:7515323-Dose-Response Relationship, Drug,
pubmed-meshheading:7515323-Endothelium, Vascular,
pubmed-meshheading:7515323-Epoprostenol,
pubmed-meshheading:7515323-Fura-2,
pubmed-meshheading:7515323-Kinetics,
pubmed-meshheading:7515323-Nitric Oxide,
pubmed-meshheading:7515323-Nitroarginine,
pubmed-meshheading:7515323-Ramipril,
pubmed-meshheading:7515323-Swine
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pubmed:year |
1994
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pubmed:articleTitle |
Enhancement of cytosolic calcium, prostacyclin and nitric oxide by bradykinin and the ACE inhibitor ramiprilat in porcine brain capillary endothelial cells.
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pubmed:affiliation |
Hoechst AG, SBU Cardiovascular Agents, Frankfurt/Main, Germany.
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pubmed:publicationType |
Journal Article
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