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 messenger that acts to release C...
| Main Authors: | , , , , |
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| Format: | Journal article |
| Language: | English |
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2011
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| _version_ | 1826274728210333696 |
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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. |
| first_indexed | 2024-03-06T22:47:52Z |
| format | Journal article |
| id | oxford-uuid:5dcf6222-c811-4e7b-82eb-4749c6585389 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T22:47:52Z |
| publishDate | 2011 |
| record_format | dspace |
| spelling | oxford-uuid:5dcf6222-c811-4e7b-82eb-4749c65853892022-03-26T17:36:34ZNAADP influences excitation-contraction coupling by releasing calcium from lysosomes in atrial myocytes.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:5dcf6222-c811-4e7b-82eb-4749c6585389EnglishSymplectic 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. |
| 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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