Linked Life Data

9000258

Source:http://linkedlifedata.com/resource/pubmed/id/9000258

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1997-5-27
pubmed:abstractText
Activated neutrophils are assumed to be one plausible cause of tissue injury in the ischaemic and reperfused myocardium. We studied the inhibitory effects of the calcium antagonists felodipine, nimodipine and verapamil on human neutrophil activation in order to elucidate the mechanisms underlying their myocardioprotective effects and to determine whether calcium antagonists with different chemical structures vary in their effect on neutrophil activation. Neutrophils were stimulated with formyl-Met-Leu-Phe (0.1 microM) or by phorbol myristate acetate (0.16 microM), and the rise in cytosolic calcium and the H2O2 production were determined. For felodipine, the inhibitory effect on granulocyte elastase release was also studied. The calcium antagonists reduced formyl-Met-Leu-Phe and phorbol myristate acetate-induced neutrophil activation in a concentration-dependent manner, the order of potency being: felodipine > nimodipine > verapamil. For felodipine, the IC50 (concentration causing 50% reduction) values were 3 x 10(-6) and 2 x 10(-6) M for the formyl-Met-Leu-Phe-induced cytosolic calcium increase and H2O2 production, respectively. The IC50-value for the phorbol myristate acetate-induced cytosolic calcium increase was 6 x 10(-6) and for H2O2 production 4 x 10(-6) M. For formyl-Met-Leu-Phe-induced granulocyte elastase release, the IC50-value was 5 x 10(-6) M. The inhibitory effect of felodipine on the phorbol myristate acetate-induced granulocyte elastase release did not exceed 50%. Nimodipine was a less potent inhibitor than felodipine for both formyl-Met-Leu-Phe- and phorbol myristate acetate-induced cell activities. Verapamil was even less potent than the other two agents. The present study demonstrates that felodipine potentially suppresses neutrophil activation at micromolar concentrations. However, this observation should not be directly extrapolated to explain the tissue protection by the compounds without evidence of profound local accumulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0901-9928
pubmed:author
pubmed:issnType
Print
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
312-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Effects of calcium blockers on the cytosolic calcium, H2O2 production and elastase release in human neutrophils.
pubmed:affiliation
Department of Cardiology, Karolinska Hospital, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Comparative Study