Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1976-10-20
pubmed:abstractText
Veratridine exerts a biphasic action on the perfused frog ventricle. The initial immediate response is a depression, which is maximal at 10(-10) M. The initial depression is followed by a late potentiation of contraction which is maximal at 10(-6) to 10(-7) M veratridine. Reduction of external calcium from 1.0 mM to 0.5 mM prevents the initial depression and allows only the potentiation of contraction to be observed. The force of contraction in 0.5 mM Ca2+ is increased by veratridine to 200% of the contraction observed at 1.0 mM Ca2+. The primary site for the enhancement of contraction in the frog ventricle by veratridine is the adrenergic nerve fibers whose increase in excitability leads to an increase in epinephrine release. The beta blocker sotalol at 10(-6) M prevents the increase in contractility by veratridine in 0.4 mM Ca2+. Calcium itself depressed potentiation of contractility by veratridine by stabilizing the adrenergic nerves and antagonizing the labilizing action of veratridine. The mode of action of veratridine on the frog ventricle is attributed to the enhancement of transmitter release from cholinergic and adrenergic nerve fibers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0301-4533
pubmed:author
pubmed:issnType
Print
pubmed:volume
221
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
190-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1976
pubmed:articleTitle
Mode of action of veratridine on perfused frog ventricle.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.