1972); radish extract, rich in saponins, stimulated GI motility in vitro and in vivo and its pharmacological activity was, at least partly, mediated by activation of muscarinic acetylcholinergic mechanism (Jung et al.
Methylisogermabul Ione isolated from radish root stimulates small bowel motility via activation of acetylcholinergic receptors.
However, NO formed as a result of iNOS upregulation during hypoxia has been found to interrupt memory process by inhibiting acetylcholinergic
gamma]-aminobutyric acid [GABA] and acetylcholinergic
neurotransmission and the endogenous opioid and cannabinoid systems).
The information mentioned above has been summarized by Lepori and colleagues, (43) and is consistent with the postulation that acetylcholinergic
mechanisms play an important hitherto unrecognized role in offsetting the hypertension and cardiac sympathetic activation caused by NOS inhibition in humans.
These findings along with those obtained in experiment 1 may suggest that acetylcholinergic
and serotoninergic neural pathways play roles in triggering metamorphosis in R.
Conclusion: The present results suggest that AJEA may specifically act on the DCLM among GI smooth muscles, and AJEA-induced DCLM contraction is likely mediated, at least, by activation of ChAT and acetylcholinergic