pubmed-article:12598585 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0017069 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0007447 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
pubmed-article:12598585 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
pubmed-article:12598585 | pubmed:issue | Pt 1 | lld:pubmed |
pubmed-article:12598585 | pubmed:dateCreated | 2003-4-2 | lld:pubmed |
pubmed-article:12598585 | pubmed:abstractText | The noradrenaline (NA)-induced cation current was investigated in neurones freshly isolated from rat cardiac parasympathetic ganglia using the nystatin-perforated patch recording configuration. Under current-clamp conditions, NA depolarized the membrane, eliciting repetitive action potentials. NA evoked an inward cation current under voltage-clamp conditions at a holding potential of -60 mV. The NA-induced current was inhibited by extracellular Ca2+ or Mg2+, with a half-maximal concentration of 13 microM for Ca2+ and 1.2 mM for Mg2+. Cirazoline mimicked the NA response, and prazosin and WB-4101 inhibited the NA-induced current, suggesting the contribution of an alpha1-adrenoceptor. The NA-induced current was inhibited by U73122, a phospholipase C (PLC) inhibitor. The membrane-permeable IP3 receptor blocker xestospongin-C also blocked the NA-induced current. Furthermore, pretreatment with thapsigargin and BAPTA-AM could inhibit the NA response while KN-62, phorbol 12-myristate 13-acetate (PMA) and staurosporine had no effect. These results suggest that NA activates the extracellular Ca2+- and Mg2+-sensitive cation channels via alpha 1-adrenoceptors in neurones freshly isolated from rat cardiac parasympathetic ganglia. This activation mechanism also involves phosphoinositide breakdown, release of Ca2+ from intracellular Ca2+ stores and calmodulin. The cation channels activated by NA may play an important role in neuronal membrane depolarization in rat cardiac ganglia. | lld:pubmed |
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pubmed-article:12598585 | pubmed:language | eng | lld:pubmed |
pubmed-article:12598585 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12598585 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12598585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:12598585 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12598585 | pubmed:month | Apr | lld:pubmed |
pubmed-article:12598585 | pubmed:issn | 0022-3751 | lld:pubmed |
pubmed-article:12598585 | pubmed:author | pubmed-author:AkaikeNorioN | lld:pubmed |
pubmed-article:12598585 | pubmed:author | pubmed-author:ItoYushiY | lld:pubmed |
pubmed-article:12598585 | pubmed:author | pubmed-author:IshibashiHito... | lld:pubmed |
pubmed-article:12598585 | pubmed:author | pubmed-author:JangIl-SungIS | lld:pubmed |
pubmed-article:12598585 | pubmed:author | pubmed-author:KimSoo YSY | lld:pubmed |
pubmed-article:12598585 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12598585 | pubmed:day | 1 | lld:pubmed |
pubmed-article:12598585 | pubmed:volume | 548 | lld:pubmed |
pubmed-article:12598585 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12598585 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12598585 | pubmed:pagination | 111-20 | lld:pubmed |
pubmed-article:12598585 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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