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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1998-7-27
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pubmed:abstractText |
The pharmacological profile and the anatomical localization of Ca2+ channels of the L-type were investigated in the human pulmonary artery to identify possible mechanisms involved in the regulation of the pulmonary vascular tone. Analysis was performed on slide-mounted frozen sections of human pulmonary artery using radioligand binding assay techniques associated with light microscope autoradiography. [3H]-Nicardipine was used as ligand. Human renal and right coronary arteries also were used as systemic reference arteries. Binding of [3H]-nicardipine to sections of human pulmonary artery was time-, temperature- and concentration-dependent, saturable and reversible. In the human pulmonary artery, the apparent equilibrium dissociation constant (Kd) was 0.12+/-0.02 nM and the maximum density of binding sites (Bmax) was 38.15+/-2.25 fmol/mg tissue. Kd values were 0.3+/-0.01 nM and 0.5+/-0.02 in the human renal artery and right coronary artery respectively. Bmax values were 248+/-16 fmol/mg tissue and 173+/-9.5 fmol/mg tissue in the human renal artery and right coronary artery respectively. The pharmacological profile of [3H]-nicardipine binding to sections of human pulmonary artery was consistent with the labeling of Ca2+ channels of the L-type. It was similar in the pulmonary artery and in the human renal and right coronary arteries. Light microscope autoradiography revealed a high density of [3H]-nicardipine binding sites within smooth muscle of the tunica media of human pulmonary artery as well as of human renal and right coronary arteries. A lower accumulation of the radioligand occurred in the tunica adventitia. No specific binding was noticeable in the tunica intima. Our data suggest that human pulmonary artery expresses Ca2+ channels of the L-type sensitive to dihydropyridines. These sites have similar affinity and lower density than those expressed by systemic arteries. The presence of Ca2+ channels of the L-type in human pulmonary artery suggests that their pharmacological manipulation may be considered in the treatment of pulmonary hypertension.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1064-1963
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
389-402
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9607402-Aged,
pubmed-meshheading:9607402-Arteries,
pubmed-meshheading:9607402-Autoradiography,
pubmed-meshheading:9607402-Calcium Channel Blockers,
pubmed-meshheading:9607402-Calcium Channels,
pubmed-meshheading:9607402-Calcium Channels, L-Type,
pubmed-meshheading:9607402-Coronary Vessels,
pubmed-meshheading:9607402-Humans,
pubmed-meshheading:9607402-Male,
pubmed-meshheading:9607402-Middle Aged,
pubmed-meshheading:9607402-Nicardipine,
pubmed-meshheading:9607402-Pulmonary Artery,
pubmed-meshheading:9607402-Renal Artery,
pubmed-meshheading:9607402-Tissue Distribution
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pubmed:year |
1998
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pubmed:articleTitle |
Density and localization of calcium channels of the L-type in human pulmonary artery.
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pubmed:affiliation |
Dipartimento di Scienze Farmacologiche e Medicina Sperimentale, Università di Camerino, Italy. amenta@cambio.unicam.it
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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