| pubmed-article:11711569 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C0002006 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C2339371 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C0178587 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:11711569 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
| pubmed-article:11711569 | pubmed:issue | Pt 1 | lld:pubmed |
| pubmed-article:11711569 | pubmed:dateCreated | 2001-11-16 | lld:pubmed |
| pubmed-article:11711569 | pubmed:abstractText | 1. Aldosterone, a major ionic homeostasis regulator, might also regulate cardiac ion currents. Using the whole-cell patch-clamp technique, we investigated whether aldosterone affects the 4-aminopyridine-sensitive transient outward K+ current (I(to1)). 2. Exposure to 100 nM aldosterone for 48 h at 37 degrees C produced a 1.6-fold decrease in the I(to1) density compared to control myocytes incubated without aldosterone. Neither the time- nor voltage-dependent properties of the current were significantly altered after aldosterone treatment. RU28318 (1 microM), a specific mineralocorticoid receptor antagonist, prevented the aldosterone-induced decrease in I(to1) density. 3. When myocytes were incubated for 24 h with aldosterone, concentrations up to 1 microM did not change I(to1) density, whereas L-type Ca(2+) current (I(Ca,L)) density increased. After 48 h, aldosterone caused a further increase in I(Ca,L). The delay in the I(to1) response to aldosterone might indicate that it occurs secondary to an increase in I(Ca,L). 4. After 24 h of aldosterone pretreatment, further co-incubation for 24 h either with an I(Ca,L) antagonist (100 nM nifedipine) or with a permeant Ca(2+) chelator (10 microM BAPTA-AM) prevented a decrease in I(to1) density. 5. After 48 h of aldosterone treatment, we observed a 2.5-fold increase in the occurrence of spontaneous Ca(2+) sparks, which was blunted by co-treatment with nifedipine. 6. We conclude that aldosterone decreases I(to1) density. We suggest that this decrease is secondary to the modulation of intracellular Ca(2+) signalling, which probably arises from the aldosterone-induced increase in I(Ca,L). These results provide new insights into how cardiac ionic currents are modulated by hormones. | lld:pubmed |
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| pubmed-article:11711569 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11711569 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11711569 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11711569 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11711569 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11711569 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:11711569 | pubmed:author | pubmed-author:VassortGG | lld:pubmed |
| pubmed-article:11711569 | pubmed:author | pubmed-author:BénitahJ PJP | lld:pubmed |
| pubmed-article:11711569 | pubmed:author | pubmed-author:GómezA MAM | lld:pubmed |
| pubmed-article:11711569 | pubmed:author | pubmed-author:PerrierEE | lld:pubmed |
| pubmed-article:11711569 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11711569 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11711569 | pubmed:volume | 537 | lld:pubmed |
| pubmed-article:11711569 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11711569 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11711569 | pubmed:pagination | 151-60 | lld:pubmed |
| pubmed-article:11711569 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11711569 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11711569 | pubmed:articleTitle | Effects of aldosterone on transient outward K+ current density in rat ventricular myocytes. | lld:pubmed |
| pubmed-article:11711569 | pubmed:affiliation | Laboratoire de Physiopathologie Cardiovasculaire, INSERM U-390, IFR3, CHU Arnaud de Villeneuve, 34295 Montpellier, France. benitah@welchlink.welch.jhu.edu | lld:pubmed |
| pubmed-article:11711569 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11711569 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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