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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1992-7-2
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pubmed:abstractText |
1. The cellular effects of alpha 1-adrenoceptor stimulation by phenylephrine were studied in the presence of propranolol in single cells isolated from the ventricles of rat hearts. 2. Phenylephrine (10-100 microM) induced a biphasic pattern of inotropism in these cells: a transient negative followed by a sustained positive inotropic effect as usually observed in cardiac tissues. 3. In Snarf-1-loaded cells, phenylephrine induced an alkalinization. This effect was reversible on wash-out and inhibited by prazosin, an alpha 1-adrenoceptor antagonist. 4. The alpha 1-adrenoceptor-mediated increase in intracellular pH (pHi) was 0.1 pH unit in HEPES buffer containing 4.4 mM-NaHCO3 and in Krebs buffer containing 25 mM-NaHCO3. 5. The alkalinization was blocked by the Na(+)-H+ antiport blocker, ethylisopropylamiloride (EIPA). 6. The recovery from an acidosis induced by a NH4Cl pre-pulse was accelerated by phenylephrine. The phenylephrine-induced alkalinization was attributed to activation of the Na(+)-H+ antiport. 7. Despite its ability to increase pHi, phenylephrine did not alter Ca2+ current amplitude and kinetics. 8. Ca2+ transients recorded in Indo-1-loaded cells were not augmented by phenylephrine. Diastolic calcium level was decreased. 9. In single skinned cells, the Ca2+ sensitivity of the contractile proteins was increased by a pre-treatment with phenylephrine even when the alpha 1-adrenoceptor-mediated alkalinizing effect had been prevented by EIPA. 10. These results lead us to propose that the alpha 1-adrenergic-induced positive inotropic response of heart muscle could result from an increased sensitivity of the myofilaments to Ca2+ ions. This alpha 1-adrenoceptor-mediated Ca2+ sensitization could result both from an intracellular alkalinization and from a direct effect on contractile proteins.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1317431-1139077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1317431-1652698,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1317431-169486,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1317431-1696995,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1317431-1698571,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
447
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
275-92
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pubmed:dateRevised |
2010-9-7
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pubmed:meshHeading |
pubmed-meshheading:1317431-Amiloride,
pubmed-meshheading:1317431-Animals,
pubmed-meshheading:1317431-Calcium,
pubmed-meshheading:1317431-Hydrogen-Ion Concentration,
pubmed-meshheading:1317431-Myocardial Contraction,
pubmed-meshheading:1317431-Myocardium,
pubmed-meshheading:1317431-Phenylephrine,
pubmed-meshheading:1317431-Rats,
pubmed-meshheading:1317431-Rats, Inbred Strains,
pubmed-meshheading:1317431-Receptors, Adrenergic, alpha
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pubmed:year |
1992
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pubmed:articleTitle |
Alpha 1-adrenergic effects on intracellular pH and calcium and on myofilaments in single rat cardiac cells.
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pubmed:affiliation |
Unité de Recherches de Physiologie Cellulaire Cardiaque, INSERM U-241, Université Paris-Sud, Orsay, France.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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