ArticleThe Journal of physiology1997
Modulation of Ca(2+)-activated Cl- currents in rabbit portal vein smooth muscle by an inhibitor of mitochondrial Ca2+ uptake.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 55 citations in OpenAlex.
- Role of ryanodine receptor 2 and FK506-binding protein 12.6 dissociation in pulmonary hypertension.The Journal of general physiology · 2023Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Mitochondrial regulation of cytosolic Ca²⁺ signals in smooth muscle.Pflugers Archiv : European journal of physiology · 2012Review
- Mitochondrial modulation of Ca2+ sparks and transient KCa currents in smooth muscle cells of rat cerebral arteries.The Journal of physiology · 2004Article
- Mitochondrial Ca2+ uptake regulates the excitability of myenteric neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- A Ca2+-permeable non-selective cation channel activated by depletion of internal Ca2+ stores in single rabbit portal vein myocytes.The Journal of physiology · 2002Article
- Calcium-dependent inhibition of L, N, and P/Q Ca2+ channels in chromaffin cells: role of mitochondria.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Mitochondrial Ca2+ homeostasis during Ca2+ influx and Ca2+ release in gastric myocytes from Bufo marinus.The Journal of physiology · 2000Article
- Physiology of rat retinal pericytes: modulation of ion channel activity by serum-derived molecules.The Journal of physiology · 1999Article
- Novel regulation of the A-type K+ current in murine proximal colon by calcium-calmodulin-dependent protein kinase II.The Journal of physiology · 1999Article
- Release of Ca2+ from the sarcoplasmic reticulum increases mitochondrial [Ca2+] in rat pulmonary artery smooth muscle cells.The Journal of physiology · 1999Article
- Hypoxia and smooth muscle function: key regulatory events during metabolic stress.The Journal of physiology · 1998Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
1. The effects of carbonyl cyanide m-chlorophenyl hydrazone (CCCP), an inhibitor of mitochondrial Ca2+ uptake, was investigated on the properties of Ca(2+)-activated chloride currents (ICl(Ca)) in rabbit portal vein smooth muscle cells using the perforated patch whole-cell voltage-clamp technique to ascertain whether this Ca2+ uptake process influences the time course of the subsarcolemmal Ca2+ signal that activates ICl(Ca). 2. In cells bathed in either physiological calcium (2 mM Cao2+) or high calcium (10 mM Cao2+) external solutions, application of CCCP (1-2 microM) evoked an inward current and prolonged the exponential decay time constant (tau) of Ca(2+)-activated Cl- 'tail' currents (Itail) evoked by Ca2+ influx through voltage-dependent calcium channels (VDCCs). The effect of CCCP on tau was greater in cells where the amplitude of Itail was relatively large and, in different cells, the effect of CCCP on tau was positively correlated with the amplitude of Itail. 3. CCCP abolished spontaneously occurring transient Ca(2+)-activated Cl- currents (STICs), but did not alter their time course before complete block. 4. Thapsigargin and cyclopiazonic acid (inhibitors of the sarcoplasmic Ca(2+)-ATPase) inhibited STICs, but did not affect the decay of Itail or STICs. 5. In conclusion, when Ca2+ enters the cell through VDCCs, the time course of the consequent Ca2+ signal in the subsarcolemmal domain containing Ca(2+)-activated chloride channels appears to be regulated by Ca2+ uptake into mitochondria. In contrast, inhibition of Ca2+ uptake by the sarcoplasmic reticulum ATPase does not seem to influence the time course of ICl(Ca).
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