ArticleThe Biochemical journal2001
Nitric oxide and cGMP activate Ca2+-release processes in rat parotid acinar cells.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 55 citations in OpenAlex.
- Effectiveness of thyme honey in the management of xerostomia in geriatric patients with end-stage renal disease: a randomized controlled clinical trial with a biochemical assessment.European journal of medical research · 2023Trial
- Deregulation of CaInternational journal of molecular sciences · 2021Article
- Production and physiological role of NO in the oral cavity.The Japanese dental science review · 2016Review
- Nitric Oxide Concentration and Other Salivary Changes after Insertion of New Complete Dentures in Edentulous Subjects.International journal of dentistry · 2016Article
- Article
- Effects of protease-activated receptors (PARs) on intracellular calcium dynamics of acinar cells in rat lacrimal glands.Histochemistry and cell biology · 2013Article
- Cyclic ADP-Ribose and NAADP in Vascular Regulation and Diseases.Messenger (Los Angeles, Calif. : Print) · 2013Article
- Article
- Identification of a novel pathway of transforming growth factor-β1 regulation by extracellular NAD+ in mouse macrophages: in vitro and in silico studies.The Journal of biological chemistry · 2012Article
- Article
- Osteocytic network is more responsive in calcium signaling than osteoblastic network under fluid flow.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012Article
- Natural killer cells regulate murine cytomegalovirus-induced sialadenitis and salivary gland disease.Journal of virology · 2012Article
- Inducible nitric oxide synthase increases secretion from inflamed salivary glands.Rheumatology (Oxford, England) · 2010Article
- Fluid Flow Induced Calcium Response in Bone Cell Network.Cellular and molecular bioengineering · 2008Article
- Defective signalling in salivary glands precedes the autoimmune response in the non-obese diabetic mouse model of sialadenitis.Clinical and experimental immunology · 2005Article
- Inhibition of calcium-calmodulin kinase restores nitric oxide production and signaling in submandibular glands of a mouse model of salivary dysfunction.British journal of pharmacology · 2004Article
- A calcium-induced calcium influx factor, nitric oxide, modulates the refilling of calcium stores in astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Atrial natriuretic peptides elevate cyclic GMP levels in primary cultures of rat ependymal cells.Neurochemical research · 2003Article
- Nitric oxide inhibits capacitative Ca2+ entry by suppression of mitochondrial Ca2+ handling.British journal of pharmacology · 2002Article
- Evidence that zymogen granules do not function as an intracellular Ca2+ store for the generation of the Ca2+ signal in rat parotid acinar cells.The Biochemical journal · 2002Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We characterized the enzymic properties of ADP-ribosyl cyclase in rat parotid acinar cells by using a fluorescence technique. ADP-ribosyl cyclase is capable of synthesizing the Ca2+ -mobilizing nucleotide cADP-ribose (cADPR) from NAD(+) and has previously been shown to be regulated by cGMP via a cGMP-dependent protein kinase (G kinase). We therefore investigated whether NO/cGMP-activated pathways are present in rat parotid acinar cells and whether NO/cGMP signalling exerts control over cellular Ca2+ signalling processes. Our results showed that stimulation of acinar cells with adrenaline, isoproterenol, substance P and NO resulted in a rise in the [cGMP]. In addition, NO induced a release of Ca2+ from intracellular ryanodine-sensitive stores via a cGMP/G-kinase-mediated process. Thus our data reveal that a rise in [cGMP], caused by either neurotransmitter or NO activation, activates a G kinase, which in turn controls Ca2+ release from ryanodine-sensitive stores. Since parotid acinar cells possess ADP-ribosyl cyclase activity, we propose a model in which cADPR is the link between NO/cGMP signalling pathways and release of Ca2+ from ryanodine-sensitive stores.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.