| pubmed-article:8058460 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C0004247 | lld:lifeskim |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C0439133 | lld:lifeskim |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C0205171 | lld:lifeskim |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:8058460 | lifeskim:mentions | umls-concept:C1611645 | lld:lifeskim |
| pubmed-article:8058460 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:8058460 | pubmed:dateCreated | 1994-9-12 | lld:pubmed |
| pubmed-article:8058460 | 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. | lld:pubmed |
| pubmed-article:8058460 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8058460 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8058460 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8058460 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8058460 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8058460 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8058460 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8058460 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8058460 | pubmed:month | May | lld:pubmed |
| pubmed-article:8058460 | pubmed:issn | 0031-6768 | lld:pubmed |
| pubmed-article:8058460 | pubmed:author | pubmed-author:LeviAA | lld:pubmed |
| pubmed-article:8058460 | pubmed:author | pubmed-author:HancoxJJ | lld:pubmed |
| pubmed-article:8058460 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8058460 | pubmed:volume | 427 | lld:pubmed |
| pubmed-article:8058460 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8058460 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8058460 | pubmed:pagination | 121-8 | lld:pubmed |
| pubmed-article:8058460 | pubmed:dateRevised | 2009-9-29 | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:meshHeading | pubmed-meshheading:8058460-... | lld:pubmed |
| pubmed-article:8058460 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8058460 | pubmed:articleTitle | The hyperpolarisation-activated current, I(f), is not required for pacemaking in single cells from the rabbit atrioventricular node. | lld:pubmed |
| pubmed-article:8058460 | pubmed:affiliation | Department of Physiology, School of Medical Sciences, Bristol, UK. | lld:pubmed |
| pubmed-article:8058460 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8058460 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8058460 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8058460 | lld:pubmed |
