ArticleBritish journal of pharmacology1996
Properties of the inhibitory junction potential in smooth muscle of the guinea-pig gastric fundus.
Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 36 citations in OpenAlex.
- Regulation of basal tone, relaxation and contraction of the lower oesophageal sphincter. Relevance to drug discovery for oesophageal disorders.British journal of pharmacology · 2008Review
- Caveolin-1 gene knockout impairs nitrergic function in mouse small intestine.British journal of pharmacology · 2005Article
- Role of protein kinase C in the excitatory action of cholinergic nerve stimulation on spontaneous activity of circular smooth muscle isolated from the guinea-pig stomach antrum.Pflugers Archiv : European journal of physiology · 2004Article
- Involvement of intramuscular interstitial cells in nitrergic inhibition in the mouse gastric antrum.The Journal of physiology · 2003Article
- The P(2)-purinoceptor antagonist suramin is a competitive antagonist at vasoactive intestinal peptide receptors in the rat gastric fundus.British journal of pharmacology · 2000Article
- Properties of gastric smooth muscles obtained from mice which lack inositol trisphosphate receptor.The Journal of physiology · 2000Article
- Cyclic GMP-associated apamin-sensitive nitrergic slow inhibitory junction potential in the hamster ileum.British journal of pharmacology · 1999Article
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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
1. In circular smooth muscle of the guinea-pig gastric fundus, transmural nerve stimulation evoked a cholinergic excitatory junction potential (e.j.p.), and blockade of the e.j.p. by atropine revealed a non-adrenergic non-cholinergic (NANC) inhibitory junction potential (i.j.p.). 2. The amplitude of the e.j.p. was increased by apamin, suramin or NGnitro-L-arginine (L-NOARG), with no significant change in the membrane potential. 3. The i.j.p. consisted of two components (fast and slow); apamin inhibited the former, nitroarginine inhibited the latter, and suramin inhibited both components. 4. Apamin inhibited the hyperpolarization produced by adenosine 5'-triphosphate (ATP) but not by vasoactive intestinal polypeptide (VIP). Suramin inhibited the hyperpolarization produced by VIP but not by ATP. The sodium nitroprusside (SNP)-induced hyperpolarization was not blocked by apamin or suramin. L-NOARG or tetrodotoxin did not inhibit the hyperpolarization produced by ATP, VIP or SNP. 5. The data did not support the hypothesis that ATP, VIP or nitric oxide (NO) is the main transmitter responsible for generation of the NANC i.j.p. in the fundus. 6. Actions of L-NOARG suggest that endogenous NO may be involved in junctional transmission, mainly as an inhibitory modulator of cholinergic transmission.
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