Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1985-4-17
pubmed:abstractText
Although the calcium antagonists verapamil, nifedipine, diltiazem and bepridil are structurally diverse, they share, to a variable extent, several pharmacologic properties. These effects are presumably the result of dose-related inhibition of transmembrane calcium ion flux through the slow channel. In diseased tissue, other routes of calcium entry may also be inhibited, and intracellular sites of action also are now strongly suspected. The calcium antagonists tend to relax vascular smooth muscle in a dose-dependent and site-specific manner. Effective coronary vasodilation is found with each agent; peripheral vasodilation is most pronounced with nifedipine, followed, in descending order of potency, by verapamil, diltiazem and bepridil. Atrioventricular conduction is also inhibited by diltiazem, bepridil and verapamil, whereas nifedipine paradoxically has no effect at therapeutic doses. The calcium antagonists also reduce muscle contractile force, but again in variable degrees. Negative inotropy is significant with verapamil and minimal with diltiazem and bepridil. Nifedipine often causes a reflex increase in contractility and heart rate. At therapeutic doses, bepridil has additional properties: it appears to affect sodium and perhaps potassium channels, producing a quinidine-like effect, and it prolongs the refractory period. Experimentally, bepridil has also been found to extend the duration of the action potential, raise the ventricular fibrillation threshold and possess both class I and class IV antiarrhythmic activity at relatively small doses. If documented clinically, bepridil may prove to be an effective antiarrhythmic as well as antianginal agent.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9149
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3C-7C
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:3872055-Action Potentials, pubmed-meshheading:3872055-Animals, pubmed-meshheading:3872055-Atrioventricular Node, pubmed-meshheading:3872055-Bepridil, pubmed-meshheading:3872055-Calcium Channel Blockers, pubmed-meshheading:3872055-Coronary Vessels, pubmed-meshheading:3872055-Diltiazem, pubmed-meshheading:3872055-Guinea Pigs, pubmed-meshheading:3872055-Heart, pubmed-meshheading:3872055-Heart Rate, pubmed-meshheading:3872055-Humans, pubmed-meshheading:3872055-Muscle, Smooth, Vascular, pubmed-meshheading:3872055-Myocardial Contraction, pubmed-meshheading:3872055-Nifedipine, pubmed-meshheading:3872055-Pyrrolidines, pubmed-meshheading:3872055-Rats, pubmed-meshheading:3872055-Vasodilation, pubmed-meshheading:3872055-Ventricular Fibrillation, pubmed-meshheading:3872055-Verapamil
pubmed:year
1985
pubmed:articleTitle
Pharmacology of calcium antagonists.
pubmed:publicationType
Journal Article, Comparative Study