The presence of many serotonin receptor subtypes enables selective drugs to be designed to therapeutically modulate gastrointestinal motility, secretion, and sensation.
The enteric nervous system (ENS) contains a plethora of neurotransmitters, which all participate in the pivotal role of ENS in controlling and modulating GI motility, secretion, and blood flow.
Cyclic adenosine 3', 5'-monophosphate (cAMP) has long been regarded as a "simple" freely diffusible second messenger, well-known for its ability to modulate multiple cellular functions such as motility, secretion, growth, metabolism, and synaptic plasticity[1], [2].
This could be of particular relevance as bile acids inhibit many bacteria and may modulate microbiota composition and also have the potential to affect major pathophysiological factors in IBS, including GI motility, secretion, and immune function (101, 102).
Intracellular regulation of calcium is an important second messenger, which is widely involved in cell motility, secretion, metabolism, and differentiation of a variety of cellular functions.
However, they are physiologically able to regulate autonomic functions such as digestive tract motility, vascular motility, secretion and absorption [1] [5].
We speculate that isoflavones, when in contact with gastric mucosa, influence prostaglandin synthesis to modulate motility.
Further analyses of the molecular mechanisms involved revealed that the P-gp inhibitor modulated parasite motility, microneme secretion and egress from the host cell, all cellular processes known to depend on Ca2+ signaling in the parasite.
The gut endocrine system produces a range of hormones that not only modulate intestinal motility and secretion but are also involved more widely in the control of metabolism.
Serotonin is a bioamine neurotransmitter primarily produced in the gut which is important for modulating intestinal motility, inflammation, and secretion [30].
