ArticleThe Journal of physiology2000
Subplasmalemmal ryanodine-sensitive Ca2+ release contributes to Ca2+-dependent K+ channel activation in a human umbilical vein endothelial cell line.
Article in The Journal of physiology, 2000. 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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12 citing papers in PubMed, 29 citations in OpenAlex.
- Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.World journal of biological chemistry · 2012Article
- Leucine zipper EF hand-containing transmembrane protein 1 (Letm1) and uncoupling proteins 2 and 3 (UCP2/3) contribute to two distinct mitochondrial Ca2+ uptake pathways.The Journal of biological chemistry · 2011Article
- The GPR55 agonist lysophosphatidylinositol acts as an intracellular messenger and bidirectionally modulates Ca2+ -activated large-conductance K+ channels in endothelial cells.Pflugers Archiv : European journal of physiology · 2011Article
- GPR55-dependent and -independent ion signalling in response to lysophosphatidylinositol in endothelial cells.British journal of pharmacology · 2010Article
- Electrophysiological characterization of store-operated and agonist-induced Ca2+ entry pathways in endothelial cells.Pflugers Archiv : European journal of physiology · 2010Article
- Vascular large conductance calcium-activated potassium channels: functional role and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2007Review
- Ca2+ refilling of the endoplasmic reticulum is largely preserved albeit reduced Ca2+ entry in endothelial cells.Cell calcium · 2007Article
- A new type of non-Ca2+-buffering Apo(a)-based fluorescent indicator for intraluminal Ca2+ in the endoplasmic reticulum.The Journal of biological chemistry · 2006Article
- Calcium-activated K+ channels of mouse beta-cells are controlled by both store and cytoplasmic Ca2+: experimental and theoretical studies.The Journal of general physiology · 2002Article
- Subplasmalemmal endoplasmic reticulum controls K(Ca) channel activity upon stimulation with a moderate histamine concentration in a human umbilical vein endothelial cell line.The Journal of physiology · 2002Article
- Capacitative Ca(2+) entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C.British journal of pharmacology · 2002Article
- Histamine-induced Ca2+ oscillations in a human endothelial cell line depend on transmembrane ion flux, ryanodine receptors and endoplasmic reticulum Ca2+-ATPase.The Journal of physiology · 2000Article
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2 authors at 1 institution in 1 country.
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Abstract
The whole-cell configuration of the patch clamp technique was used to assess the involvement of ryanodine-sensitive Ca2+ release (RsCR) in histamine-activated Ca2+-dependent K+ (KCa) channels in the human umbilical vein endothelial cell line EA.hy926. Histamine (10 microM) induced a transient outward current that reached 18.9 +/- 5.5 pA pF-1 at +20 mV. This current was diminished by 1 mM tetraethylammonium or 50 nM iberiotoxin, by 90 % and 80 %, respectively, suggesting that this current results from the stimulation of large-conductance KCa (BKCa) channels. In about 50 % of the cells tested, stimulation of RsCR with 200 nM ryanodine initiated a small outward current that was also sensitive to iberiotoxin. Following the ryanodine-mediated RsCR, the potency of 10 microM histamine to activate KCa channels was reduced by about 60 %. In agreement, an inhibition of RsCR with 25 microM ryanodine diminished KCacurrent in response to histamine by about 70 %. The effect of 100 microM histamine on KCa channel activity was not reduced by previous RsCR with 200 nM ryanodine, or by an inhibition of RsCR by 25 microM ryanodine. Histamine (10 microM)-induced Ca2+ elevation was reduced by 30 % following ryanodine-mediated RsCR, whereas no inhibition occurred in the case of 100 microM histamine stimulation. In cells treated with 10 microM nocodazole for 16 h to collapse the superficial endoplasmic reticulum, 200 nM ryanodine failed to initiate any KCa current. Furthermore, the inhibitory effect of previous RsCR on 10 microM histamine-induced KCa current was not obtained in nocodazole-treated cells. Our data suggest that during moderate cell stimulation (10 microM histamine), subplasmalemmal RsCR greatly contributes to the activation of KCa channels in endothelial cells. Thus, the function of the subplasmalemmal Ca2+ control unit (SCCU) described previously must be extended as a regulator for KCa channels.
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