ArticleThe Journal of physiology2002
Comparative capacitative calcium entry mechanisms in canine pulmonary and renal arterial smooth muscle cells.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Long-Term Hypoxia Negatively Influences CaFrontiers in physiology · 2021Article
- AMP-activated protein kinase inhibits Kv 1.5 channel currents of pulmonary arterial myocytes in response to hypoxia and inhibition of mitochondrial oxidative phosphorylation.The Journal of physiology · 2016Article
- Conformation of ryanodine receptor-2 gates store-operated calcium entry in rat pulmonary arterial myocytes.Cardiovascular research · 2016Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Maternal high-altitude hypoxia and suppression of ryanodine receptor-mediated Ca2+ sparks in fetal sheep pulmonary arterial myocytes.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Long-term maternal hypoxia: the role of extracellular Ca2+ entry during serotonin-mediated contractility in fetal ovine pulmonary arteries.Reproductive sciences (Thousand Oaks, Calif.) · 2011Article
- Protein kinases modulate store-operated channels in pulmonary artery smooth muscle cells.Journal of biomedical science · 2011Article
- TRPC1 and STIM1 mediate capacitative Ca2+ entry in mouse pulmonary arterial smooth muscle cells.The Journal of physiology · 2009Article
- Enhanced capacitative calcium entry and sarcoplasmic-reticulum calcium storage capacity with advanced age in murine mesenteric arterial smooth muscle cells.Experimental gerontology · 2009Article
- Maturation of intracellular calcium homeostasis in sheep pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- Store-operated calcium entry in vascular smooth muscle.British journal of pharmacology · 2008Review
- Role of InsP3 and ryanodine receptors in the activation of capacitative Ca2+ entry by store depletion or hypoxia in canine pulmonary arterial smooth muscle cells.British journal of pharmacology · 2007Article
- Ca2+ signalling in urethral interstitial cells of Cajal.The Journal of physiology · 2006Review
- Mobilization of sarcoplasmic reticulum stores by hypoxia leads to consequent activation of capacitative Ca2+ entry in isolated canine pulmonary arterial smooth muscle cells.The Journal of physiology · 2005Article
- Role of basal extracellular Ca2+ entry during 5-HT-induced vasoconstriction of canine pulmonary arteries.British journal of pharmacology · 2005Article
- Non-selective cationic channels of smooth muscle and the mammalian homologues of Drosophila TRP.The Journal of physiology · 2004Review
- Pharmacological profile of store-operated channels in cerebral arteriolar smooth muscle cells.British journal of pharmacology · 2003Article
- Caffeine inhibits InsP3 responses and capacitative calcium entry in canine pulmonary arterial smooth muscle cells.Vascular pharmacologyArticle
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7 authors.
Funding
Abstract
Experiments were performed to determine whether capacitative Ca(2+) entry (CCE) can be activated in canine pulmonary and renal arterial smooth muscle cells (ASMCs) and whether activation of CCE parallels the different functional structure of the sarcoplasmic reticulum (SR) in these two cell types. The cytosolic [Ca(2+)] was measured by imaging fura-2-loaded individual cells. Increases in the cytosolic [Ca(2+)] due to store depletion in pulmonary ASMCs required simultaneous depletion of both the inositol 1,4,5-trisphosphate (InsP(3))- and ryanodine (RY)-sensitive SR Ca(2+) stores. In contrast, the cytosolic [Ca(2+)] rises in renal ASMCs occurred when the SR stores were depleted through either the InsP(3) or RY pathways. The increase in the cytosolic [Ca(2+)] due to store depletion in both pulmonary and renal ASMCs was present in cells that were voltage clamped and was abolished when cells were perfused with a Ca(2+)-free bathing solution. Rapid quenching of the fura-2 signal by 100 microM Mn(2+) following SR store depletion indicated that extracellular Ca(2+) entry increased in both cell types and also verified that activation of CCE in pulmonary ASMCs required the simultaneous depletion of the InsP(3)- and RY-sensitive SR Ca(2+) stores, while CCE could be activated in renal ASMCs by the depletion of either of the InsP(3)- or RY-sensitive SR stores. Store depletion Ca(2+) entry in both pulmonary and renal ASMCs was strongly inhibited by Ni(2+) (0.1-10 mM), slightly inhibited by Cd(2+) (200-500 microM), but was not significantly affected by the voltage-gated Ca(2+) channel (VGCC) blocker nisoldipine (10 microM). The non-selective cation channel blocker Gd(3+) (100 microM) inhibited a portion of the Ca(2+) entry in 6 of 18 renal but not pulmonary ASMCs. These results provide evidence that SR Ca(2+) store depletion activates CCE in parallel with the organization of intracellular Ca(2+) stores in canine pulmonary and renal ASMCs.
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