ArticleBritish journal of pharmacology2000
Nitrergic relaxation of the mouse gastric fundus is mediated by cyclic GMP-dependent and ryanodine-sensitive mechanisms.
Article in British journal of pharmacology, 2000. 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, 35 citations in OpenAlex.
- Docosahexaenoic acid and eicosapentaenoic acid strongly inhibit prostanoid TP receptor-dependent contractions of guinea pig gastric fundus smooth muscle.Pharmacology research & perspectives · 2022Article
- Caffeine impairs gastrointestinal function in newborn rats.Pediatric research · 2015Article
- Regulation of gastrointestinal motility by Ca2+/calmodulin-stimulated protein kinase II.Archives of biochemistry and biophysics · 2011Review
- Block of inhibitory junction potentials and TREK-1 channels in murine colon by Ca2+ store-active drugs.The Journal of physiology · 2008Article
- Gastric motility in soluble guanylate cyclase alpha 1 knock-out mice.The Journal of physiology · 2007Article
- Study on the cyclic GMP-dependency of relaxations to endogenous and exogenous nitric oxide in the mouse gastrointestinal tract.British journal of pharmacology · 2007Article
- Effect of modulation of serotonergic, cholinergic, and nitrergic pathways on murine fundic size and compliance measured by ultrasonomicrometry.American journal of physiology. Gastrointestinal and liver physiology · 2006Article
- NANC inhibitory neurotransmission in mouse isolated stomach: involvement of nitric oxide, ATP and vasoactive intestinal polypeptide.British journal of pharmacology · 2003Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. Ryanodine-sensitive, Ca(2+) release ('Ca(2+) sparks') from the sarcoplasmic reticulum (SR) can activate plasmalemmal Ca(2+)-activated K(+) channels (K(Ca)) to cause membrane hyperpolarization and smooth muscle relaxation. Since cyclic guanosine monophosphate (cyclic GMP) can modulate Ca(2+) spark activity, the aim of the present study was to determine if Ca(2+) spark-like events are involved in NO-dependent, NANC relaxations to electrical field stimulation (EFS) of mouse, longitudinal smooth muscle of the gastric fundus in isolated strips contracted to approximately 40% of their maximum contraction. 2. NANC relaxations to EFS were almost abolished by both the NO synthase inhibitor, N(G)-nitro-L-arginine (L-NOARG; 100 microM) and the guanylate cyclase inhibitor, 1-H-oxodiazol-[1,2,4]-[4,3-alpha] quinoxaline-1-one (ODQ; 10 microM). Also, ODQ abolished relaxations to the NO donor, sodium nitroprusside (SNP; 1 nM - 30 microM). NANC relaxations and SNP-evoked relaxations were both partly ryanodine (10 microM)- and nifedipine (0.3 microM)-sensitive, but in each case, the inhibitory effects of ryanodine and nifedipine were additive. 3. Apamin (1 microM), charybdotoxin (0.1 microM), iberiotoxin (0.1 microM), tetraethylammonium (TEA; 1 mM), glibenclamide (10 microM) and 4-aminopyridine (1 mM) had no effect on either NANC- or SNP-evoked relaxations, the latter of which were also unaffected by high extracellular K(+) (68 mM). 4. Caffeine (0.1 - 1 mM) caused concentration-dependent relaxations of gastric fundus which were inhibited by ryanodine but unaffected by L-NOARG. 5. Relaxation to ATP (30 microM) was abolished by nifedipine, partly inhibited by apamin and ryanodine, but was unaffected by L-NOARG. 6. In conclusion, the results of the present study show that nitrergic relaxations in the mouse longitudinal gastric fundus occur via a cyclic GMP-activated ryanodine-sensitive mechanism, which does not appear to involve activation of K(+) channels.
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