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• W2071995297 abstract "To study the contribution of the Na + ‐Ca 2+ exchanger to Ca 2+ regulation and its interaction with the sarcoplasmic reticulum (SR), changes in cytoplasmic Ca 2+ concentration ([Ca 2+ ] c ) were measured in single, voltage clamped, smooth muscle cells. Increases in [Ca 2+ ] c were evoked by either depolarisation (−70 mV to 0 mV) or by release from the SR by caffeine (10 m m ) or flash photolysis of caged Ins P 3 (Ins P 3 ). Depletion of the SR of Ca 2+ (verified by the absence of a response to caffeine and Ins P 3 ) by either ryanodine (50 μ m ), to open the ryanodine receptors (RyRs), or thapsigargin (500 n m ) or cyclopiazonic acid (CPA, 10 μ m ), to inhibit the SR Ca 2+ pumps, reduced neither the magnitude of the Ca 2+ transient nor the relationship between the influx of and the rise in [Ca 2+ ] c evoked by depolarisation. This suggested that Ca 2+ ‐induced Ca 2+ release (CICR) from the SR did not contribute significantly to the depolarisation‐evoked rise in [Ca 2+ ] c . However, although Ca 2+ was not released from it, the SR accumulated the ion following depolarisation since ryanodine and thapsigargin each slowed the rate of decline of the depolarisation‐evoked Ca 2+ transient. Indeed, the SR Ca 2+ content increased following depolarisation as assessed by the increased magnitude of the [Ca 2+ ] c levels evoked each by Ins P 3 and caffeine, relative to controls. The increased SR Ca 2+ content following depolarisation returned to control values in approximately 12 min via Na + ‐Ca 2+ exchanger activity. Thus inhibition of the Na + ‐Ca 2+ exchanger by removal of external Na + (by either lithium or choline substitution) prevented the increased SR Ca 2+ content from returning to control levels. On the other hand, the Na + ‐Ca 2+ exchanger did not appear to regulate bulk average Ca 2+ directly since the rates of decline in [Ca 2+ ] c , following either depolarisation or the release of Ca 2+ from the SR (by either Ins P 3 or caffeine), were neither voltage nor Na + dependent. Thus, no evidence for short term (seconds) control of [Ca 2+ ] c by the Na + ‐Ca 2+ exchanger was found. Together, the results suggest that despite the lack of CICR, the SR removes Ca 2+ from the cytosol after its elevation by depolarisation. This Ca 2+ is then removed from the SR to outside the cell by the Na + ‐Ca 2+ exchanger. However, the exchanger does not contribute significantly to the decline in bulk average [Ca 2+ ] c following transient elevations in the ion produced either by depolarisation or by release from the store." @default.
• W2071995297 created "2016-06-24" @default.
• W2071995297 creator A5030229064 @default.
• W2071995297 creator A5041961469 @default.
• W2071995297 creator A5049936609 @default.
• W2071995297 creator A5072011531 @default.
• W2071995297 date "2002-01-01" @default.
• W2071995297 modified "2023-09-26" @default.
• W2071995297 title "Ca²⁺ regulation in guinea‐pig colonic smooth muscle: the role of the Na⁺‐Ca²⁺ exchanger and the sarcoplasmic reticulum" @default.
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• W2071995297 doi "https://doi.org/10.1113/jphysiol.2001.013039" @default.
• W2071995297 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2290079" @default.
• W2071995297 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11790813" @default.
• W2071995297 hasPublicationYear "2002" @default.
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