ArticleThe Biochemical journal2003
Nitric oxide co-ordinates the activities of the capacitative and non-capacitative Ca2+-entry pathways regulated by vasopressin.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 57 citations in OpenAlex.
- Resveratrol inhibits CaEnvironmental health and preventive medicine · 2020Article
- Effects of protease-activated receptors (PARs) on intracellular calcium dynamics of acinar cells in rat lacrimal glands.Histochemistry and cell biology · 2013Article
- Protein kinases modulate store-operated channels in pulmonary artery smooth muscle cells.Journal of biomedical science · 2011Article
- Inhibition of serine/threonine phosphatase enhances arachidonic acid-induced [Ca2+]i via protein kinase A.American journal of physiology. Cell physiology · 2009Article
- Arachidonic acid and ion channels: an update.British journal of pharmacology · 2008Review
- Novel role for polycystin-1 in modulating cell proliferation through calcium oscillations in kidney cells.Cell proliferation · 2008Article
- Discrete influx events refill depleted Ca2+ stores in a chick retinal neuron.The Journal of physiology · 2008Article
- Different phospholipase-C-coupled receptors differentially regulate capacitative and non-capacitative Ca2+ entry in A7r5 cells.The Biochemical journal · 2005Article
- Ca2+ signaling, intracellular pH and cell volume in cell proliferation.The Journal of membrane biology · 2005Review
- Evidence against reciprocal regulation of Ca2+ entry by vasopressin in A7r5 rat aortic smooth-muscle cells.The Biochemical journal · 2005Article
- Stimulation of cellular free Ca2+ elevation and inhibition of store-operated Ca2+ entry by kazinol B in neutrophils.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
- Non-selective cationic channels of smooth muscle and the mammalian homologues of Drosophila TRP.The Journal of physiology · 2004Review
- Intracellular calcium signals and control of cell proliferation: how many mechanisms?Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In A7r5 vascular smooth muscle cells vasopressin, via arachidonic acid, regulates two Ca(2+)-entry pathways. Capacitative Ca(2+) entry (CCE), activated by empty Ca(2+) stores, is inhibited by arachidonic acid, and non-capacitative Ca(2+) entry (NCCE) is stimulated by it. This reciprocal regulation ensures that all Ca(2+) entry is via NCCE in the presence of vasopressin, while CCE mediates a transient Ca(2+) entry only after removal of vasopressin. We demonstrate that type III NO synthase (NOS III) is expressed in A7r5 cells and that NO inhibits CCE. Inhibition of CCE by vasopressin requires NOS III and the requirement lies downstream of arachidonic acid. Activation of soluble guanylate cyclase by NO and subsequent activation of protein kinase G are required for inhibition of CCE. Stimulation of NCCE by vasopressin also requires NOS III, but the stimulation is neither mimicked by cGMP nor blocked by inhibitors of soluble guanylate cyclase or protein kinase G. We conclude that arachidonic acid formed in response to vasopressin stimulates NOS III. NO then directly stimulates Ca(2+) entry through NCCE and, via protein kinase G, it inhibits CCE. The additional amplification provided by the involvement of guanylate cyclase and protein kinase G ensures that CCE will always be inhibited when vasopressin activates NCCE.
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