Linked Life Data

2175796

Source:http://linkedlifedata.com/resource/pubmed/id/2175796

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1991-2-7
pubmed:abstractText
Caffeine (0.1-10 mM) produced a biphasic effect on Na(+)-K+ ATPase activity in the rat heart sarcolemmal preparations. The Na(+)-K+ ATPase activity was stimulated by about 25% at low concentrations (0.1-1 mM), whereas the enzyme was inhibited by about 25% at higher concentrations (10 mM) of caffeine. The stimulatory effect of 1 mM caffeine was associated with about 30% increase in the Vmax value for Na(+)-K+ ATPase, whereas the depressant action of 10 mM caffeine was associated with an increase of the Km value from 1.4 to 2.1 mM ATP. The Na(+)-induced Ca++ release from the sarcolemmal vesicles was stimulated with caffeine in a concentration-dependent manner; about 80% increase in the activity was observed at 0.1 mM caffeine. The apparent Ka (millimolar Na+) values for the Na(+)-induced Ca++ release were about 17 and 6 in the absence and presence of 1 mM caffeine, respectively. However, the sarcolemmal Na(+)-dependent Ca++ uptake and ATP-independent Ca++ binding were not affected, whereas the ATP-dependent Ca++ accumulation and Ca+(+)-stimulated ATPase activities were depressed by 1 to 10 mM caffeine. This agent at concentrations of 0.1 to 10 mM produced a biphasic effect on the contractile activity of the isolated perfused rat heart. The initial transient positive inotropic (30-60%) effect was followed by a sustained negative inotropic (50-80%) response of the drug; the delayed decrease in contractile force was associated with a significant increase (35-50%) in the resting tension. The initial positive inotropic effect of caffeine was dependent on the concentration of Ca++ (0.2-3 mM) in the perfusion medium; however, this response was attenuated either by lowering the concentration of Na+ from 140 to 35 mM or by different concentrations (0.5-1 mM) of amiloride in the medium.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
255
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1188-94
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:2175796-Adenosine Triphosphatases, pubmed-meshheading:2175796-Adenosine Triphosphate, pubmed-meshheading:2175796-Animals, pubmed-meshheading:2175796-Biological Transport, Active, pubmed-meshheading:2175796-Ca(2+) Mg(2+)-ATPase, pubmed-meshheading:2175796-Caffeine, pubmed-meshheading:2175796-Calcium, pubmed-meshheading:2175796-Cardiotonic Agents, pubmed-meshheading:2175796-Dose-Response Relationship, Drug, pubmed-meshheading:2175796-Heart, pubmed-meshheading:2175796-Kinetics, pubmed-meshheading:2175796-Male, pubmed-meshheading:2175796-Myocardial Contraction, pubmed-meshheading:2175796-Myocardium, pubmed-meshheading:2175796-Rats, pubmed-meshheading:2175796-Rats, Inbred Strains, pubmed-meshheading:2175796-Sarcolemma, pubmed-meshheading:2175796-Sodium, pubmed-meshheading:2175796-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:2175796-Verapamil
pubmed:year
1990
pubmed:articleTitle
Cardiac sarcolemma as a possible site of action of caffeine in rat heart.
pubmed:affiliation
Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Manitoba, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't