ArticleThe Journal of physiology2001
Functional coupling between nitric oxide synthesis and VIP release within enteric nerve terminals of the rat: involvement of protein kinase G and phosphodiesterase 5.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 28 citations in OpenAlex.
- CamKIIα and VPAC1 Expressions in the Caudal Trigeminal Nucleus of Rats After Systemic Nitroglycerin Treatment: Interaction with Anandamide.Life (Basel, Switzerland) · 2025Article
- Intestinal and neuronal myenteric adaptations in the small intestine induced by a high-fat diet in mice.BMC gastroenterology · 2015Article
- PKA-dependent activation of the vascular smooth muscle isoform of KATP channels by vasoactive intestinal polypeptide and its effect on relaxation of the mesenteric resistance artery.Biochimica et biophysica acta · 2008Article
- Nitric oxide-NGF mediated PPTA/SP, ADNP, and VIP expression in the peripheral nervous system.Journal of molecular neuroscience : MN · 2007Article
- Inhibitory pathways in the circular muscle of rat jejunum.British journal of pharmacology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The subcellular mechanisms involved in the effect of nitric oxide (NO) on the release of vasoactive intestinal polypeptide (VIP) were examined in synaptosomes isolated from rat small intestine. 2. VIP release was stimulated by the NO donor SNAP (10(-7)-10(-4) M) in an oxyhaemoglobin-sensitive manner. The presence of the guanylate cyclase inhibitor ODQ (10(-5) M), or inhibition of protein kinase G (PKG) by KT 5823 (3 x 10(-6) M) or Rp-8Br-PET-cGMPS (5 x 10(-7) M), antagonized the SNAP-induced VIP release, suggesting a regulatory role of PKG, confirming previously published data from enteric ganglia. This finding was further supported by the fact that direct PKG activation by the stable cGMP analogue 8-pCPT-cGMP stimulated VIP secretion to the same extent as SNAP. 3. Basal VIP secretion was enhanced in the presence of zaprinast, an inhibitor of cGMP-dependent phosphodiesterase 5 (PDE 5), suggesting a functional role of PDE 5 in NO-cGMP signalling. Supportive evidence for this finding was obtained by demonstration of the presence of PDE 5 using RT-PCR. 4. Stimulation of endogenous NO production by L-arginine was also effective in releasing VIP. The effect was abolished in the presence of KT 5823, but was insensitive to oxyhaemoglobin (10(-3) M), suggesting that an interaction between NO and VIP is likely to occur within the same nerve terminal rather than between terminals. 5. NO synthesis was not affected by VIP (10(-8)-10(-5) M), suggesting that there is no feedback regulation between the NO and the VIP pathways. 6. These findings support the notion that an anatomical and functional interrelationship exists between NO and VIP in enteric nerve terminals and that complex signalling mechanisms involving PKG and PDE 5 contribute to NO-induced VIP release.
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