pubmed-article:18467629 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C0086376 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C0449560 | lld:lifeskim |
pubmed-article:18467629 | lifeskim:mentions | umls-concept:C1521805 | lld:lifeskim |
pubmed-article:18467629 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:18467629 | pubmed:dateCreated | 2008-6-6 | lld:pubmed |
pubmed-article:18467629 | pubmed:abstractText | We examined the effect of alpha(1)-adrenoceptor subtype-specific stimulation on L-type Ca2+ current (I(Ca)) and elucidated the subtype-specific intracellular mechanisms for the regulation of L-type Ca2+ channels in isolated rat ventricular myocytes. We confirmed the protein expression of alpha(1A)- and alpha(1B)-adrenoceptor subtypes at the transverse tubules (T-tubules) and found that simultaneous stimulation of these 2 receptor subtypes by nonsubtype selective agonist, phenylephrine, showed 2 opposite effects on I(Ca) (transient decrease followed by sustained increase). However, selective alpha(1A)-adrenoceptor stimulation (> or =0.1 micromol/L A61603) only potentiated I(Ca), and selective alpha(1B)-adrenoceptor stimulation (10 mumol/L phenylephrine with 2 micromol/L WB4101) only decreased I(Ca). The positive effect by alpha(1A)-adrenoceptor stimulation was blocked by the inhibition of phospholipase C (PLC), protein kinase C (PKC), or Ca2+/calmodulin-dependent protein kinase II (CaMKII). The negative effect by alpha(1B)-adrenoceptor stimulation disappeared after the treatment of pertussis toxin or by the prepulse depolarization, but was not attributable to the inhibition of cAMP-dependent pathway. The translocation of PKCdelta and epsilon to the T-tubules was observed only after alpha(1A)-adrenoceptor stimulation, but not after alpha(1B)-adrenoceptor stimulation. Immunoprecipitation analysis revealed that alpha(1A)-adrenoceptor was associated with G(q/11), but alpha(1B)-adrenoceptor interacted with one of the pertussis toxin-sensitive G proteins, G(o). These findings demonstrated that the interactions of alpha(1)-adrenoceptor subtypes with different G proteins elicit the formation of separate signaling cascades, which produce the opposite effects on I(Ca). The coupling of alpha(1A)-adrenoceptor with G(q/11)-PLC-PKC-CaMKII pathway potentiates I(Ca). In contrast, alpha(1B)-adrenoceptor interacts with G(o), of which the betagamma-complex might directly inhibit the channel activity at T-tubules. | lld:pubmed |
pubmed-article:18467629 | pubmed:language | eng | lld:pubmed |
pubmed-article:18467629 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18467629 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:18467629 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18467629 | pubmed:month | Jun | lld:pubmed |
pubmed-article:18467629 | pubmed:issn | 1524-4571 | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:SasakiHiroyuk... | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:MorimotoSatos... | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:KuriharaSatos... | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:HongoKenichiK | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:KusakariYoich... | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:KomukaiKimiak... | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:ShinjiHitomiH | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:ObataToruT | lld:pubmed |
pubmed-article:18467629 | pubmed:author | pubmed-author:O-UchiJinJ | lld:pubmed |
pubmed-article:18467629 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18467629 | pubmed:day | 6 | lld:pubmed |
pubmed-article:18467629 | pubmed:volume | 102 | lld:pubmed |
pubmed-article:18467629 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18467629 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18467629 | pubmed:pagination | 1378-88 | lld:pubmed |
pubmed-article:18467629 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:18467629 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18467629 | pubmed:articleTitle | Interaction of alpha1-adrenoceptor subtypes with different G proteins induces opposite effects on cardiac L-type Ca2+ channel. | lld:pubmed |
pubmed-article:18467629 | pubmed:affiliation | Department of Cell Physiology, The Jikei University School of Medicine, 3-25-8 Nishi-Shimbashi, Minato-ku, Tokyo 105-8461 Japan. o-uchi@jikei.ac.jp | lld:pubmed |
pubmed-article:18467629 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18467629 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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