pubmed-article:1714581 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1714581 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:1714581 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:1714581 | lifeskim:mentions | umls-concept:C0022009 | lld:lifeskim |
pubmed-article:1714581 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:1714581 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
pubmed-article:1714581 | pubmed:issue | 16 | lld:pubmed |
pubmed-article:1714581 | pubmed:dateCreated | 1991-9-18 | lld:pubmed |
pubmed-article:1714581 | pubmed:abstractText | The cAMP-dependent regulation of ion channels was studied by using the whole-cell configuration of the patch clamp technique. In isolated cardiac ventricular myocytes, the beta-adrenergically regulated Cl- current (ICl) exhibited an unusual dependence on Na+, such that replacement of extracellular Na+ with compounds such as tetramethylammonium, choline, Tris, or N-methyl-D-glucamine resulted in a reduction in current amplitude without changing the reversal potential. Replacement of extracellular Na+ with tetramethylammonium also reduced the magnitude of the beta-adrenergically enhanced Ca2+ current and delayed rectifier K+ current, suggesting that removal of Na+ was affecting the cAMP pathway that regulates all three currents. Replacement of extracellular Na+ also reduced ICl that was stimulated by (i) direct activation of adenylate cyclase with forskolin, (ii) inhibition of phosphodiesterase with 3-isobutyl-1-methylxanthine, (iii) exposure to the membrane-permeable cAMP derivative 8-bromoadenosine 3',5'-cyclic monophosphate, or (iv) direct phosphorylation of the channel with protein kinase A catalytic subunit. This suggests that the Na+ dependence is at a point beyond the activation of protein kinase A. The Na+ dependence of ICl regulation could not be explained by changes in intracellular Ca2+. However, the sensitivity of the ICl to changes in extracellular Na+ depended significantly on the intracellular Na+ concentration, suggesting that intracellular Na+ plays an important role in the cAMP-dependent regulation of ion channels. | lld:pubmed |
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pubmed-article:1714581 | pubmed:language | eng | lld:pubmed |
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pubmed-article:1714581 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1714581 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1714581 | pubmed:month | Aug | lld:pubmed |
pubmed-article:1714581 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:1714581 | pubmed:author | pubmed-author:HumeJ RJR | lld:pubmed |
pubmed-article:1714581 | pubmed:author | pubmed-author:HarveyR DRD | lld:pubmed |
pubmed-article:1714581 | pubmed:author | pubmed-author:JureviciusJ... | lld:pubmed |
pubmed-article:1714581 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1714581 | pubmed:day | 15 | lld:pubmed |
pubmed-article:1714581 | pubmed:volume | 88 | lld:pubmed |
pubmed-article:1714581 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1714581 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1714581 | pubmed:pagination | 6946-50 | lld:pubmed |
pubmed-article:1714581 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:1714581 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1714581 | pubmed:articleTitle | Intracellular Na+ modulates the cAMP-dependent regulation of ion channels in the heart. | lld:pubmed |
pubmed-article:1714581 | pubmed:affiliation | Department of Physiology, University of Nevada School of Medicine, Reno 89557. | lld:pubmed |
pubmed-article:1714581 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1714581 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1714581 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:1714581 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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