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Last Updated: 3 years ago

Possible Interaction: Acetylcholine and Arachidonic Acid

Research Papers that Mention the Interaction

Since AA is a natural ligand for PPARα, ACh stimulates PPARα probably via AA.
Biomedical research  •  2016  |  View Paper
Thus, ACh stimulates AA accumulation via an [Ca2+]i increase, which activates PPARα, leading to enhancement of Ca2+‐regulated exocytosis in antral mucous cells.
Experimental physiology  •  2010  |  View Paper
ACh stimulates arachidonic acid (AA) release from membrane phospholipids of vascular endothelial cells (ECs).
American journal of physiology. Heart and circulatory physiology  •  2006  |  View Paper
Acetylcholine stimulates the release of endothelium-derived arachidonic acid ( AA ) metabolites including prostacyclin and epoxyeicosatrienoic acids (EETs), which relax coronary arteries.
American journal of physiology. Heart and circulatory physiology  •  2005  |  View Paper
The basal release of arachidonic acid was initially increased by infusion of acetylcholine and became lower than the initial basal levels after 30 min of infusion.
Naunyn-Schmiedeberg's Archives of Pharmacology  •  2004  |  View Paper
Since muscarinic activation triggers AA production and we now observed that AA enhances ACh release, it is proposed that AA may act as a facilitatory retrograde messenger in hippocampal cholinergic muscarinic transmission as it has been proposed to act in glutamatergic transmission.
Brain Research  •  1999  |  View Paper
These results indicate that arachidonic acid endogenously formed under weak stimulation of NMDA receptors contributes to the regulation of the evoked release of [3H]‐acetylcholine by facilitating GABAergic transmission and that this process is more important in striosomes than in the matrix.
Synapse  •  1999  |  View Paper
Moreover, the neuronal arachidonic acid production evoked by glutamate was potentiated by acetylcholine.
Glia  •  1994  |  View Paper
ACh increases [3H]arachidonic acid release in esophageal but not in lower esophageal sphincter (LES) muscle.
The American journal of physiology  •  1994  |  View Paper
Arachidonic acid (10 uM) perfused into an adrenal gland of the rat … caused a significant inhibition of CA secretion evoked by ACh (5.32×10−3 M), DMPP (10−4 M) and muscarine (10−4 M) … did not affect that induced by excess K+ (5.6×10−2 M).
The perfusion of arachidonic acid along with indomethacin (30 uM), which is an inhibitor of cyclooxygenase, for 20 min attenuated markedly CA secretory effect evoked by ACh , DMPP and muscarine while it did not influence that by excess K+.
The Korean journal of internal medicine  •  1993  |  View Paper
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