Motility gastrointestinal system

Muscarinic M3 receptor Antagonist Acute (gastrointestinal system) Reduced GI motility Darifenacin26... 

Aromatic plants are commonly administered as an infusion or tea, and thus are delivered directly to the site of action, i.e. the gastrointestinal system [216, 224]. Basically, aromatic plants and their EOs exert their digestive action by inhibiting gastric motility (antispasmodics), releasing of bile from the gall bladder (choler-... 

Mentha arvensis L. M. haplocalyx Briq. China Menthol, menthone, menthyl acetate.33 Stimulate gastrointestinal tract motility and central nervous system, dilate peripheral blood vessels. Increase sweat gland secretion. 

For almost one century, acetylcholine has been recognized as a neurotransmitter both in the central nervous system and the peripheral nervous system. In the peripheral nervous system, acetylcholine has been identified as the neurotransmitter of autonomic ganglia and the neuromuscular junction. Acetylcholine is involved in different peripheral functions such as heart rate, blood flow, gastrointestinal tract motility, and sweat production and smooth muscle activity. In the CNS, cholinergic neurotransmission plays a crucial role in a variety of CNS functions including sensory perception, motor function, cognitive processing, memory, arousal, attention, sleep, nociception, motivation, reward, mood, and psychosis. 

DOMPERIDONE, METOCLOPRAMIDE ANTIMUSCARINICS i efficacy of domperidone on gut motility by antimuscarinics Some effects of metodopramide are considered to be due to t release of ACh and t sensitivity of the cholinergic receptors to ACh. Antimuscarinics prevent the effects on muscarinic receptors The gastrointestinal effects of metodopramide will be impaired, while the antiemetic effects may not be. Thus, concurrent use with antimuscarinics is not advised because of effects on the gastrointestinal system... 

Primarily effects on the gastrointestinal system. These include decreased bowel motility and decreased gastric acid secretion. It is also believed that there is a vestibular component to the emetic action of opiate drugs. 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

The parasympathetic nervous system is capable of maintaining gastrointestinal motility, etc., even when connections to the central nervous system have been... 

There are a number of side-effects of opiates that are due to their actions on opiate receptors outside the central nervous system. Opiates constrict the pupils by acting on the oculomotor nucleus and cause constipation by activating a maintained contraction of the smooth muscle of the gut which reduces motility. This diminished propulsion coupled with opiates reducing secretion in the gut underlie the anti-diarrhoeal effect. Opiates contract sphincters throughout the gastrointestinal tract. Although these effects are predominantly peripheral in origin there are central contributions as well. Morphine can also release histamine from mast cells and this can produce irritation and broncho-spasm in extreme cases. Opiates have minimal cardiovascular effects at therapeutic doses. 

Cardiovascular Effects. In a recent report on the clinical treatment of phenol poisoning, Langford et al. (1998) provide a summary of a case report in which a woman accidentally consumed an ounce of 89% phenol which had been mistakenly been given to her in preparation for an in-office procedure. Her immediate reaction upon consuming the phenol was to clutch her throat and collapse, and within 30 minutes she was comatose and had gone into respiratory arrest. Treatment was initiated with an endotracheal intubation. Ventilation with a bag and mask led to the detection of a lamp oil odor. Within an hour she developed ventricular tachycardia which responded to cardioversion however, she subsequently developed (in the first 24 hours) supraventricular and ventricular dysrhythmias, metabolic acidosis, and experienced a grand mal seizure. After a 15-day hospital stay, she was completely recovered with no evidence of impaired motility or compromised gastrointestinal or cardiovascular systems. 

Atropine and scopolamine have antispasmodic effects on the gastrointestinal tract. It partly inhibits vagal influence in the gut, reducing motility. However, the enteric nervous system also employs serotonin and dopamine, so parasympathetic innervation plays a modulatory role. 

Dopamine is an intermediate product in the biosynthesis of noradrenaline. Furthermore it is an active transmitter by itself in basal ganglia (caudate nucleus), the nucleus accumbens, the olfactory tubercle, the central nucleus of the amygdala, the median eminence and some areas in the frontal cortex. It is functionally important, for example in the extra-pyramidal system and the central regulation of emesis. In the periphery specific dopamine receptors (Di-receptors) can be found in the upper gastrointestinal tract, in which a reduction of motility is mediated, and on vascular smooth muscle cells of splanchnic and renal arteries. Beside its effect on specific D-receptors, dopamine activates, at higher concentrations, a- and -adrenoceptors as well. Since its clinical profile is different from adrenaline and noradrenaline there are particular indications for dopamine, like situations of circulatory shock with a reduced kidney perfusion. Dopamine can dose-dependently induce nausea, vomiting, tachyarrhythmia and peripheral vasoconstriction. Dopamine can worsen cardiac ischaemia. 

Additional effects of nicotine include an increase in gastric acid secretion and an increase in the tone and motility of the gastrointestinal tract. These effects are produced because of the predominance of cholinergic input to these effector systems. 

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