Linked Life Data

8058460

Source:http://linkedlifedata.com/resource/pubmed/id/8058460

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1994-9-12
pubmed:abstractText
The atrioventricular node (AVN) is vital for cardiac function. One of its properties is that it can act as a pacemaker for the ventricles if the sinoatrial node fails. This study investigates the role of the hyperpolarisation-activated inward current (I(f)) in generating pacemaker activity in morphologically normal single cells isolated from the rabbit AVN. Whole-cell patch-clamp recordings show that 80%-90% of AVN myocytes do not possess I(f), but nevertheless generate spontaneous action potentials with normal pacemaker depolarisations before each action potential upstroke. We have termed this type of cell "type 1". A small proportion (10%-20%) of spontaneously active AVN cells (type 2) do exhibit I(f). A 100 nM solution of isoprenaline increased the action potential rate of type 1 cells by 31%. In these cells isoprenaline did not activate any I(f) whereas in type 2 cells it clearly increased the amplitude of I(f). Manganese at 2 mM also increased the amplitude of I(f) in type 2 cells, but did not reveal I(f) in type 1 cells. We conclude that, whilst I(f) may play a role in modulating pacemaker activity in type 2 cells, in the majority of AVN cells (type 1) pacemaker depolarisation normally occurs in the complete absence of I(f). Furthermore, the inability of both isoprenaline and Mn to reveal I(f) in type 1 cells suggests that I(f) channels may be absent in these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
427
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
121-8
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
The hyperpolarisation-activated current, I(f), is not required for pacemaking in single cells from the rabbit atrioventricular node.
pubmed:affiliation
Department of Physiology, School of Medical Sciences, Bristol, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't