ArticlePflugers Archiv : European journal of physiology2008
Acetylcholine-induced Ca2+ oscillations are modulated by a Ca2+ regulation of InsP3R2 in rat portal vein myocytes.
Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Central role of IPCell death & disease · 2019Article
- Functional Role of Intracellular Calcium Receptor Inositol 1,4,5-Trisphosphate Type 1 in Rat Hippocampus after Neonatal Anoxia.PloS one · 2017Article
- The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Biochimica et biophysica acta · 2015Review
- Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries.Pflugers Archiv : European journal of physiology · 2013Article
- Article
- Inositol 1,4,5-trisphosphate receptor subtype-specific regulation of calcium oscillations.Neurochemical research · 2011Review
- The decrease of expression of ryanodine receptor sub-type 2 is reversed by gentamycin sulphate in vascular myocytes from mdx mice.Journal of cellular and molecular medicine · 2009Article
- Mechanism of asynchronous Ca(2+) waves underlying agonist-induced contraction in the rat basilar artery.British journal of pharmacology · 2009Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oscillations of cytosolic Ca2+ levels are believed to have important roles in various metabolic and signalling processes in many cell types. Previously, we have demonstrated that acetylcholine (ACh) evokes Ca2+ oscillations in vascular myocytes expressing InsP3R1 and InsP3R2, whereas transient responses are activated in vascular myocytes expressing InsP3R1 alone. The molecular mechanisms underlying oscillations remain to be described in these native smooth muscle cells. Two major hypotheses are proposed to explain this crucial signalling activity: (1) Ca2+ oscillations are activated by InsP3 oscillations; and (2) Ca2+ oscillations depend on the regulation of the InsP3R by both InsP3 and Ca2+. In the present study, we used a fluorescent InsP3 biosensor and revealed that ACh induced a transient InsP3 production in all myocytes. Moreover, steady concentrations of 3F-InsP3, a poorly hydrolysable analogue of InsP3, and pharmacological activation of PLC evoked Ca2+ oscillations. Increasing cytosolic Ca2+ inhibited the ACh-induced calcium oscillations but not the transient responses and strongly reduced the 3F-InsP3-evoked Ca2+ response in oscillating cells but not in non-oscillating cells. These results suggest that, in native vascular myocytes, ACh-induced InsP3 production is transient and Ca2+ oscillations depend on a Ca2+ modulation of InsP3R2.
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