Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1989-8-11
pubmed:abstractText
The effects of alpha adrenoceptor stimulation with noradrenaline were investigated in rat ventricular myocytes after blockade of beta receptors with propranolol (1 microM). At room temperature and low stimulation frequency (0.5 Hz), noradrenaline evoked a phentolamine-sensitive increase in contraction amplitude by 22%. The action potentials of myocytes were prolonged. When the sodium current was inactivated by depolarization in whole-cell voltage clamp experiments, noradrenaline caused a small, but highly variable increase in net inward current and shifted the current-voltage relation between -30 and -5 mV to the hyperpolarizing direction. These effects were absent when K+ currents were inhibited by Cs+ substitution. After inhibition of the Ca++ current with Cd++ (0.1 mM), noradrenaline decreased the peak transient outward current; it reduced the steady-state outward current in a concentration-dependent manner (pD2 value, 6.9), but had no effect on the amplitude of the transient component of outward current. Noradrenaline reduced holding current at -40 mV. The inward branch of the inward rectifier was not affected. The noradrenaline-induced changes in membrane currents were significantly smaller in the presence of phentolamine (10 microM). They are therefore considered to be mediated by alpha adrenoceptor stimulation. The reduction in outward currents can explain the prolongation in action potential duration which could contribute to the increase in contractility.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
250
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
364-70
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Alpha adrenoceptor stimulation reduces outward currents in rat ventricular myocytes.
pubmed:affiliation
Department of Pharmacology, University of Essen, W. Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't