| pubmed-article:10066919 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0022009 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:10066919 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:10066919 | pubmed:dateCreated | 1999-7-16 | lld:pubmed |
| pubmed-article:10066919 | pubmed:abstractText | 1. We studied the effect of overexpression of the beta2-adrenergic receptor (beta2-AR) in the heart on ion channel currents in single cells isolated from hearts of fetal and neonatal transgenic and wild-type mice. The beta2-AR transgene construct was under the control of the murine alpha-myosin heavy chain (alpha-MHC) promoter, and ion channel activity was measured at distinct developmental stages using whole-cell and perforated patch clamp techniques. 2. We found no change in L-type Ca2+ channel current (ICa) density in early embryonic stages (E11-13) of beta2-AR transgenic positive (TG+) mice, but significant increases in ICa density in intermediate (E14-16, 152 %) and late (E17-19, 173.7 %) fetal and neonatal (1 day post partum, 161 %) TG+ compared with transgenic negative (TG-) mice. This increase in ICa was accompanied by a negative shift in the peak of the current-voltage relationship in TG+ mice. 3. Transient (< 3 min) or prolonged (16-24 h) exposure of TG- neonatal stage myocytes to 8-Br-cAMP (300 microM) increased ICa density and caused a shift in the current-voltage relationship to a similar extent to that seen in TG+ mice. In TG+ myocytes, 8-Br-cAMP had no effect. Exposure of TG+ cells to Rp-cAMPS reversed both the shift in voltage dependence and reduced the peak current density observed in these myocytes. We concluded from these results that the L-type Ca2+ channel is maximally modulated by cAMP-dependent protein kinase (PKA) in TG+ mice and that the alpha-MHC promoter is functional in the ventricle as early as embryonic day 14. 4. In contrast, we found that slow delayed rectifier K+ channels were not changed significantly at any of the developmental stages studied by the overexpression of beta2-ARs compared with TG- mice. The sensitivity of murine slow delayed rectifier K+ channels to cAMP was tested by both transient and prolonged exposure to 8-Br-cAMP (300 microM), which increased the slow delayed rectifier K+ channel current (IK,s) density to a similar extent in both TG- and TG+ neonatal myocytes. In addition, we found that there was no difference in the concentration dependence of the response of ICa and IK,s to 8-Br-cAMP. 5. Thus, overexpression of the beta2-AR in the heart results in distinct modulation of ICa, but not IK,s, and this is not due to differences in the 8-Br-cAMP sensitivity of the two channels. Instead, these results are consistent with both compartmentalization of beta2-AR-controlled cAMP and distinct localization of L-type Ca2+ and slow delayed rectifier K+ channels. This cAMP is targeted preferentially to the L-type Ca2+ channel and is not accessible to the slow delayed rectifier K+ channel. | lld:pubmed |
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| pubmed-article:10066919 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10066919 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10066919 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10066919 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10066919 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10066919 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10066919 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:10066919 | pubmed:author | pubmed-author:LefkowitzR... | lld:pubmed |
| pubmed-article:10066919 | pubmed:author | pubmed-author:KassR SRS | lld:pubmed |
| pubmed-article:10066919 | pubmed:author | pubmed-author:AnRR | lld:pubmed |
| pubmed-article:10066919 | pubmed:author | pubmed-author:KochW JWJ | lld:pubmed |
| pubmed-article:10066919 | pubmed:author | pubmed-author:HeathB MBM | lld:pubmed |
| pubmed-article:10066919 | pubmed:author | pubmed-author:HigginsJ PJP | lld:pubmed |
| pubmed-article:10066919 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10066919 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:10066919 | pubmed:volume | 516 ( Pt 1) | lld:pubmed |
| pubmed-article:10066919 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10066919 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10066919 | pubmed:pagination | 19-30 | lld:pubmed |
| pubmed-article:10066919 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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