NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes
In atrial myocytes, the sarcoplasmic reticulum (SR) has an essential role in regulating the force of contraction as a consequence of its involvement in excitation-contraction coupling (ECC). Nicotinic acid adenine dinucleotide phosphate (NAADP) is a Ca 2+ mobilizing messenge...
| Auteurs principaux: | , , , , |
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| Format: | Journal article |
| Langue: | English |
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2011
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| _version_ | 1826302718803705856 |
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| author | Collins, T Bayliss, R Churchill, G Galione, A Terrar, D |
| author_facet | Collins, T Bayliss, R Churchill, G Galione, A Terrar, D |
| author_sort | Collins, T |
| collection | OXFORD |
| description | In atrial myocytes, the sarcoplasmic reticulum (SR) has an essential role in regulating the force of contraction as a consequence of its involvement in excitation-contraction coupling (ECC). Nicotinic acid adenine dinucleotide phosphate (NAADP) is a Ca 2+ mobilizing messenger that acts to release Ca 2+ from an acidic store in mammalian cells. The photorelease of NAADP in atrial myocytes increased Ca 2+ transient amplitude with no effect on accompanying action potentials or the L-type Ca 2+ current. NAADP-AM, a cell permeant form of NAADP, increased Ca 2+ spark amplitude and frequency. The effect on Ca 2+ spark frequency could be prevented by bafilomycin A1, a vacuolar H +-ATPase inhibitor, or by disruption of lysosomes by GPN. Bafilomycin prevented staining of acidic stores with LysoTracker red by increasing lysosomal pH. NAADP-AM also produced an increase in the lysosomal pH, as detected by a reduction in LysoSensor green fluorescence. These effects of NAADP were associated with an increase in the amount of caffeine-releasable Ca 2+ in the SR and may be regulated by β-adrenoceptor stimulation with isoprenaline. These observations are consistent with a role for NAADP in regulating ECC in atrial myocytes by releasing Ca 2+ from an acidic store, which enhances SR Ca 2+ release by increasing SR load. © 2011 Elsevier Ltd. |
| first_indexed | 2024-03-07T05:51:48Z |
| format | Journal article |
| id | oxford-uuid:e9222fa2-5a17-4cfc-a898-bc80c76a9907 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T05:51:48Z |
| publishDate | 2011 |
| record_format | dspace |
| spelling | oxford-uuid:e9222fa2-5a17-4cfc-a898-bc80c76a99072022-03-27T10:52:05ZNAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytesJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:e9222fa2-5a17-4cfc-a898-bc80c76a9907EnglishSymplectic Elements at Oxford2011Collins, TBayliss, RChurchill, GGalione, ATerrar, DIn atrial myocytes, the sarcoplasmic reticulum (SR) has an essential role in regulating the force of contraction as a consequence of its involvement in excitation-contraction coupling (ECC). Nicotinic acid adenine dinucleotide phosphate (NAADP) is a Ca 2+ mobilizing messenger that acts to release Ca 2+ from an acidic store in mammalian cells. The photorelease of NAADP in atrial myocytes increased Ca 2+ transient amplitude with no effect on accompanying action potentials or the L-type Ca 2+ current. NAADP-AM, a cell permeant form of NAADP, increased Ca 2+ spark amplitude and frequency. The effect on Ca 2+ spark frequency could be prevented by bafilomycin A1, a vacuolar H +-ATPase inhibitor, or by disruption of lysosomes by GPN. Bafilomycin prevented staining of acidic stores with LysoTracker red by increasing lysosomal pH. NAADP-AM also produced an increase in the lysosomal pH, as detected by a reduction in LysoSensor green fluorescence. These effects of NAADP were associated with an increase in the amount of caffeine-releasable Ca 2+ in the SR and may be regulated by β-adrenoceptor stimulation with isoprenaline. These observations are consistent with a role for NAADP in regulating ECC in atrial myocytes by releasing Ca 2+ from an acidic store, which enhances SR Ca 2+ release by increasing SR load. © 2011 Elsevier Ltd. |
| spellingShingle | Collins, T Bayliss, R Churchill, G Galione, A Terrar, D NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes |
| title | NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes |
| title_full | NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes |
| title_fullStr | NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes |
| title_full_unstemmed | NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes |
| title_short | NAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes |
| title_sort | naadp influences excitation contraction coupling by releasing calcium from lysosomes in atrial myocytes |
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