Introduction to control of alimentary tract Flashcards
Role of ANS
The autonomic nervous system innervates the gut in terms of extrinsic parasympathetic (e.g. vagal) and sympathetic (e.g. splachnic) supply and then there is the intrinsic enteric nervous system.
parasympathetic will promote the digestive function and therefore digestive activity, secretions (gallbladder) and relax the rectum
sympathetic will inhibit digestive activity and stimulate the release of glucose via the liver
Autonomic innervation of the gut
sight + smell of food have an effect on stomach -> send message down to the stomach via the vagal nerves therefore the stomach relaxes before the food gets there due to anticipation
as food make it way to the duodenum -> splanchnic nerve will promote activity within the GI tract
food making its way to the end of the stomach + food in SI -> contraction due to Ach and substance P/K
The contraxtion will be behind the bolus of food to move the food along so the other end needs to relac therefore VIP and NO will be released
Smooth muscle cells with receptors able to release neurotransmitters that will help to modulate peristaltic reflex
Innervation of the gut
The gut is innervated by various parts of the nervous system.
There are vagus afferent fibres from the gut muscle and mucosa which travel to the brain and effect fibres which communicate with the ENS.
There is also communication from the spinal cord to the ENS by the splanchinic nerves. The splanchnic nerves carry afferent sympathetic neurones to the spinal cord and efferent neurones to the ENS.
The ENS doesn’t have to rely on the CNS, ENS can send its own signals to the gut muscle and mucosa
ANS enables food storage in stomach
Empty stomach = 50ml Receptive relaxation of fundus and body of stomach Stomach accommodates 1.5L of food Parasympathetic nerves Vagus inhibitory fibres
Relaxation of the reservoir (fundus) is mediated by reflexes and can be differentiated into 3 types and name one component mediator
receptive (mechanical stimulation of pharynx – mechanoreceptors, sight),
adaptive (vagal innervation (NO/VIP), tension of stomach)
feedback (nutrients, CCK).
other mediators for the relaxation of the stomach
Briefly, the receptive, adaptive and feedback-relaxation of the stomach are mediated by non-adrenergic, non-cholinergic (NANC) mechanisms (i.e., inhibition involving NO, VIP, etc.) as well as by reflex chains involving release of noradrenaline. When the stomach is ready to receive the food, very early on, noradrenaline is released from the sympathetic nerve fibres which helps the stomach to relax. For a single best answer question, the correct answer will depend on the list of possible answers.
PACAP: pituitary adenylate cyclase (AC)-activating peptide (secretin family of peptides): isolated from pituitary and shown to stimulate adenylate cyclase AC activity in the anterior pituitary
High levels in brain, but also found in gut – myenteric and submucosal ganglia
Mediates neuronal regulation of gastric acid secretion; intestinal motility
Stimulates relaxation of colonic smooth muscle and stimulates pancreatic secretions; stimulates insulin and glucagon secretion in humans.
Recap: functions of ANS enable storage of food in stomach
Vagus inhibitory fibres allow the release of NO and VIP
Mechanical stimuli within pharynx due to food in mouth called receptive relaxation which allows storage of food (stomach prepares)
Adaptive relaxation -> presence of food within the fundus allow relaxation to occur
Feedback -> if fat in food component, the partially digested food will make its way to the duodenum and the duodenum mucosa will pick it up that fat is there therefore it will feedback to higher centres of the brain (the vagus centre) which send a message down to say no need to put food here as CCK is release which allows adaptive relaxation to occur and you feel fuller for longer
CCK -> also promote the contraction of the gall bladder to allow bile duct secretion which will emulsify fat
Effect of selective vagotomy
decreased accomodation of stomach + decreased compliance
ANS enables movement of partially digested food into duodenum
Ripples of contraction move the food towards the antrum (thicker muscle layer) - where grinding will occur
Pyloric sphincter is often relaxed but closes upon arrival of peristaltic wave - don’t want too much food entering duodenum as its a smaller reservoir
Repulsion of chyme causes the opening of pyloric sphincter
Small partially digested material is squirted through the pyloric sphincter into duodenum
Repulsion of antral contents backwards towards the body allows mixing/grinding
food enetring stomach and effect when entering duodenum
Cranial nerves + proximal contraction + motilin hormone are important for contraction
GRP (gastin releasing peptide) to release gastrin
CCK for contraction of gall bladder + relaxation of fundus and longer acccomadation is promoted
Whatever happens in the duodenum wtheter that is acid, protein or fat content, will feedback to the proximal end of the stomach -> duodenum is distended by the passage of the periodic squirting of partially digested food _> feedback will occur e.g. can’t cope no more due to detection of acid so controls how much bi-carbonate is produced
What are horomones?
Hormones are carried in the blood from their site of production to their target site
All hormones produced by the gut are peptides (sequence of amino acids)
Neurocrine communication
sensory neuron -> interneuron -> secretomotorneuron to secrete neurotransmitter e.g. Ach where it binds to a receptor and get an effect
Ach -> contraction + secretion as it promotes acid secretion
Endocrine communication
The Ach secretiob initiated by sight of food, smell of food, taste of food and food in stomach -> neuronal process therefore gastrin-mediated + Ach-mediated acid secretion
Secretomotor neurons release Ach which binds to receptos on Parietal cells (musacarinic receptors). Ach can bind to ECL cells to promote histamine secretion too. The histamine will bind to H2 receptors on pareital cells to release Hcl
GRP causes the secretion of gastrin from G cells which will travel in the blood. It can have an effect on the parietal cells directly or it can bind to target cells on the ECL cells.
When gastrin binds to this, it promotes the secretion of histamine from those cells which promote acid secretion from parietal cells as histamine has receptors (H2) which mediate acid secretion
Other endocrine hormones that have an effect
oestradiol and progesterone can reduce the gut transition time
Paracrine control and example
paracrine agents go via the interstitial fluid to adjacent cells
When too much acid production from G cell, the D cell will secrete somatostatin which will inhibit the G cell. This is dependent on high levels of H+ as H+ will bind to the D cell to secrete somatostatin
Neural control
There is both parasympathetic and sympathetic supply to the gut.
A large amount of parasympathetic is from the vagal nerve (vagal afferents and efferents) as well as there being spinal afferents and efferents from the sympathetic system (mainly splanchnic nerves). (afferents going towards CNS, efferents towards the gut).
Vagus nerve afferents innervate the lower oesophagus, fundic region and duodenal area.
What is the vago-vagal reflex?
It is reflex circuit within the GIT
A reflex in which both the afferent (“sensory”) and efferent (“motor”) axons are in the vagus nerve trunk
Pathway is via the brain stem (medulla)
The vago-vagal reflex is active during the relaxation of the stomach in response to swallowing food.
What is the vago-vagal pathway?
Control of accommodation
Coordination of contraction/relaxation of GIT
Food when consumed will stimulate the mechano receptor which will stimulate the vagal afferent fibres. The brain will decide it wants to increase motility/secretion
Vagal afferents from the gut enter into the medulla -> NTS -> DMVN -> vagal efferent
The short post-gangilionic vagal nerve releases Ach at the target tissue of the gut, which effects secretion and motility of the gut.
Enteric nervous system or local reflex
Two nerve fibres are intrinsic to the gut: Myenteric plexus (Auerbach’s plexus): motor function Submucosal plexus (Meissner’s plexus): intestinal secretions
Reflexly regulate GI function entirely within the wall of the gut
Connected to CNS by parasympathetic and sympathetic fibres, but can function autonomously without these connections
Those effects are mediated entirely by the enteric nervous system (the third component of the ANS)-has a similar number of neurons (100 million) as the spinal cord
Neurotransmitters: ACh, NA, 5-HT, GABA, ATP, NO
Auerbach’s plexus and Meissner’s plexus
Auerbach’s plexus has both parasympathetic and sympathetic input whereas the Meissner’s plexus has only parasympathetic fibres and provides secretomotor innervation to the mucosa nearest the lumen of the gut
submucosal/meissner plexus surrounds the submucosa and is beneath the circular muscle -> closer to lumen for secretions
auerbach/myentric plexus is beneath the logituduinal muscle and between that and circular muscle -> for motor control
Auerbach’s plexus (myentric plexus)
Most prominent plexus
Cholinergic innervation ↑ gastric motility and secretion
Adrenergic stimulation ↓ gastric motility and secretion
Colo-colonic reflex
presence of food or food products/distension of the stomach increase motility of the colon in response – again it is due to stretch in the stomach and by-products of digestion in the small intestine
Metabolic – type of food eaten
Rate of emptying is dependent upon the material’s ability to be absorbed
Carbohydrates emptied quickly into duodenum
Proteins – slow emptying
Fatty foods – even slower due to emulsification in duodenum which is a time dependent process
Fatty acids in the duodenum → ↓ in gastric emptying by increasing the contractility of pyloric sphincter therefore accomodation will continue to occur
Peristalsis
Slower in large intestine compared to small intestine
Wave of propulsive contractions moves contents of gut towards the anus
Distension initiates contraction -> caused by the presence of a bolus of food -> mechano-receptors have vagal innervation to allow peristalsis to occur
Vagal inhibitory and excitatory fibres control movement (control the contraction and relaxation of gut smooth muscles) -> in a coordinated fashion (longtidunal muscle contract + circular muscle relax on the recieving end but the opposite happens on other end so coordinated action)
