ArticleGastroenterology2013
Cell-specific deletion of nitric oxide-sensitive guanylyl cyclase reveals a dual pathway for nitrergic neuromuscular transmission in the murine fundus.
Article in Gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Cellular and molecular mechanisms underlying aging-related gastric neuromuscular dysfunction.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025Review
- Loss of soluble guanylyl cyclase in platelets contributes to atherosclerotic plaque formation and vascular inflammation.Nature cardiovascular research · 2022Article
- Calcium transients in intramuscular interstitial cells of Cajal of the murine gastric fundus and their regulation by neuroeffector transmission.The Journal of physiology · 2022Article
- CaAdvances in experimental medicine and biology · 2022Article
- The effect of Xenin25 on spontaneous circular muscle contractions of rat distal colon in vitro.Physiological reports · 2021Article
- Functions of Muscarinic Receptor Subtypes in Gastrointestinal Smooth Muscle: A Review of Studies with Receptor-Knockout Mice.International journal of molecular sciences · 2021Review
- Excitatory cholinergic responses in mouse colon intramuscular interstitial cells of Cajal are due to enhanced CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Activity within specific enteric neurochemical subtypes is correlated with distinct patterns of gastrointestinal motility in the murine colon.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- CaThe Journal of physiology · 2019Article
- Colonic Transit Disorder Mediated by Downregulation of Interstitial Cells of Cajal/Anoctamin-1 in Dextran Sodium Sulfate-induced Colitis Mice.Journal of neurogastroenterology and motility · 2019Article
- Nitric oxide and its role as a non-adrenergic, non-cholinergic inhibitory neurotransmitter in the gastrointestinal tract.British journal of pharmacology · 2019Review
- Optogenetic and chemogenetic techniques for neurogastroenterology.Nature reviews. Gastroenterology & hepatology · 2018Review
- Inhibitory Neural Regulation of the CaFrontiers in physiology · 2018Article
- Inhibitory responses mediated by vagal nerve stimulation are diminished in stomachs of mice with reduced intramuscular interstitial cells of Cajal.Scientific reports · 2017Article
- Change in the Interstitial Cells of Cajal and nNOS Positive Neuronal Cells with Aging in the Stomach of F344 Rats.PloS one · 2017Article
- Article
- Regulation of Gastrointestinal Smooth Muscle Function by Interstitial Cells.Physiology (Bethesda, Md.) · 2016Review
- CrossTalk opposing view: Interstitial cells are not involved and physiologically important in neuromuscular transmission in the gut.The Journal of physiology · 2016Article
- CrossTalk proposal: Interstitial cells are involved and physiologically important in neuromuscular transmission in the gut.The Journal of physiology · 2016Article
- Rebuttal from Raj K Goyal.The Journal of physiology · 2016Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsIt is not clear how nitric oxide (NO) released from enteric neurons relaxes gastrointestinal (GI) smooth muscle. In analogy to the vascular system, NO might directly induce relaxation of smooth muscle cells (SMCs) by acting on its receptor, NO-sensitive guanylyl cyclase (NO-GC). Alternatively, intermediate cells, such as the interstitial cells of Cajal (ICCs), might detect nitrergic signals to indirectly regulate smooth muscle tone, and thereby regulate the motor function of the GI tract. We investigated the role of ICCs and SMCs in nitrergic relaxation using mice with cell-specific disruption of the gene encoding the β1 subunit of NO-GC (GUCY1B3).
methodsWe created mice that lack NO-GC specifically in SMCs (SM-guanylyl cyclase knockout [GCKO]), ICCs (ICC-GCKO), or both (SM/ICC-GCKO). We investigated the effects of exogenous and endogenous NO on murine fundus using isometric force studies. Total gut transit time was measured to monitor the functional consequences of NO-GC deletion on GI motility in vivo.
resultsNO-GC is expressed in ICC and SMC. Deletion of the NO receptor from SMCs incompletely reduced NO-induced fundus relaxation, which was hardly affected after ICC-specific deletion. Gut transit time did not change in SM-GCKO or ICC-GCKO mice compared with control mice. However, nitrergic relaxation was not observed in SM/ICC-GCKO mice, which had increased gut transit time compared with controls.
conclusionsIn mice, NO-GC is the only NO receptor to relax the fundus; deletion of NO-GC from the combination of SMCs and ICCs blocks nitrergic signaling. Therefore, ICCs and SMCs jointly mediate the relaxant effect of enteric NO.
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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.