I ninja nerds in this video we're going to talk about gastric secretions others three important phases of gaseous secretion cephalic gastric and intestinal in this video we're primarily going to discuss the cephalic in the gastric phase okay but again I want you to remember that when we talk about this gastric secretions have this in a two part video we're gonna focus in this one on the cephalic in the gastric okay so phallic and then we'll have gastric in this one too and another video we will discuss the intestinal phase okay so in this video we're
gonna talk about the cephalic and we're gonna talk about the gastric now when we talk about this gastric secretion we have to know that cephalic actually accounts for about one third about one third of the gastric juice that is secreted by the stomach okay so four out of the gastric secretions secreting the gastric acid the cephalic phase accounts for one third the gastric phase accounts for the significant two-thirds of the amount okay so this one is going to be the main one for gastric acid secretion now in order for us to talk about these guys
we have to get a little bit of an idea about what are some of the things that can stimulate and inhibit these phases so let's first do the stimulatory effects so for the cephalic phase there is four really important stimuli four really important stimuli one is going to be the sight of food okay so the sight of food whenever you see the food it hits the redness sends the information eventually back to the occipital lobe which is the cerebral cortex from that we can send that information to the hypothalamus or even down to the medulla
okay so that's one thing the second thing is the thought of food you know the thought of food can originate maybe within even the prefrontal cortex and then from there the prefrontal cortex can send the information down to the hypothalamus and then even down to the medulla another one is the smell of food the smell of food you know you actually have different types of odor and chemicals from the different types of food substances it can hit the olfactory receptors get traveled up through the olfactory nerves up to the olfactory bulb and then eventually it'll
get then sent to different types of cortex right the cerebral cortex from there and then can go to the hypothalamus and then it can even go to the medulla and the last one is going to be the taste of food okay all the really cool thing about the cephalic phase is the gastric juice that our stomach is producing is its producing it before foodies even entered into the stomach that's what it's so interesting about this phase same thing with taste we have taste buds and they're located on the tongue they pick up the different taste
chemicals they send the information down the different cranial nerves for example that's the anterior two-thirds that would be carried by the facial nerve if it's gonna be the posterior one-third that be care about the glossopharyngeal nerve it even a little bit apart of the posterior aspect of the pharynx there's even a little bit of the vagus nerve there too so these are the important things but one thing I want you to remember here for the cephalic phase is all this actual gastric juice that we're producing within the cephalic phase occurs before food even enters into
the stomach okay so now let's see how these things these stimuli influence the gastric secretion all right so first off we say that the these certain things can cause stimulation to the cerebral cortex right so let's assume that these are some cerebral cortex neurons from here the cerebral cortex neurons can then send information down to the hypothalamus so let's assume right here this area right here let's just put here a patch of grey matter here this patch of gray matter here is called the hypothalamus from this the hypothalamus can send these descending axons downwards and
come down to a special nucleus located within the medulla you know the medulla had this beautiful purple nucleus and this beautiful purple nucleus here is called the dorsal nucleus of Vegas so what does this guy here call them and I abbreviated D and V dorsal nucleus of Vegas now if we stimulate this guess what's gonna happen the vagus nerve is going to come out here of the medulla and it's actually gonna run out through the jugular foramen and then eventually it'll come down to the stomach when it goes down to the stomach it can go
to all parts of the stomach so it can go to you know there's different parts of the stomach here for example this part here the top part of the stomach we refer to this part here as the cardia of the stomach okay so we refer to this part here is the cardia this part here this big lumpy region here this is referred to as the fundus okay then so here we'll kind of do it like this this part there is the fundus and then this part here for let's say from about here to about there
this is called the corpus or the body of the stomach and then this other part right here is called the Antrim and then you have the last part of it here where there's a sphincter and that is called the pylorus now this vagus nerve goes to all parts of the stomach okay so it's going to all different parts of the stomach but what it's doing is it's going to specific cells that we're going to talk about in this video and that is going to be called the parietal cells those are the main ones we'll also
talk about the chief cells - but when it goes to these different parietal cells and chief cells it stimulates these guys to make a specific chemical and that is called hydrochloric acid HCL and the other chemical that we're going to make is called pepsin imogen but pepsinogen had a specific ph and we'll talk about that can become activated and turned into a very beautiful and active digesting enzyme called pepsin these are the main contents of the gastric juice and we'll talk about a little bit of the mucus too that forms the mucosal barrier protecting our
epithelial cells protecting us from like peptic ulcers okay so that's what we know then we know that these four things can stimulate structures within the cerebral cortex so that's something to note this is this is the cerebral cerebral cortex alright now once that happens we know that this will send information to live both alamos down to the vagus nerve and come down here via the efferent fibers of the vagus nerve to trigger the hydrochloric acid and pepsin secretion the next thing that you should be asking yourself is okay I know that this is a stimulatory
vincible what's the inhibitory events the inhibitory events here are going to be anything that activates the sympathetic nervous system is honestly that simple anything that activates the sympathetic nervous system I mean it could be stress it could be emotional upset whatever it might be anything that activates the sympathetic nervous system will then inhibit the gastric secretions you know how okay we come over here you know in the actual spinal cord anywhere around the area of like t1 to l2 there's these sympathetic fibers the preganglionic fibers what they do is is they can give off these
preganglionic fibers and this is gonna be like a splanchnic nerve here right so this is going to be a splanchnic nerve this we're here we'll call splanchnic nerve and primarily this would be like the greaters plactic nerve if you really wanted to know that okay but anyway this is going to come down here and it's also going to try to inhibit any of those secretions so it's going to try to inhibit those gastric acid secretions that is his goal so these guys the parasympathetic their goal is to increase the actual hydrochloric acid secretion and pepsin
secretion whereas the sympathetic is going to try to inhibit the vagal nerve stimulation and by doing that by inhibiting the vagal nerve stimulation you thereby decrease the hydrochloric acid production let's do this in blue to be consistent you'll try to decrease the hydrochloric acid production and decrease the pepsin production okay the sympathetic nervous system doesn't directly act on the parietal cells and it doesn't necessarily it can't act on the to the chief' cells but the big thing that I want you to remember here is when the sympathetic nervous system is activated it in the parasympathetic
nervous system can no longer act on this parietal cells in chief cells okay there is dual innervation but only one system can operate or dominate at that point time so therefore if the parasympathetic isn't stimulating there's gonna be no gastric juices there okay that talks about in the simplest form this is a phallic phase okay so now we got to talk about the gastric phase the gash your face is a really important phase because this one is going to account for this as you can see two thirds of the gastro do secretion now same thing
here what are the stimuli for the gastric fees the stimuli for this one is distension okay so distension now distension is basically a fancy word for stretch okay now here's what I want you remember there's stretch receptors that are located all around the actual stomach and particularly generally we can find them like in the submucosa or you you can even find them in really high concentrations in the muscularis externa so if for whatever reason there is a lot of food because if you have to think about a gastric phase as food is now in the
stomach the cephalic phases there was no food in the stomach and we were producing gastric juices preparing for the food but now food is in the stomach and it's occupying the stomach and stretching the stomach walls if that happens we have these stretch receptors this red neuron here and what this guy will do is is he will come up and look what he can do he can stimulate the vagus nerve if he stimulates the vagus nerve what will the vagus nerve do it'll trigger the hydrochloric acid production and pepsin secretion it's in that so awesome
it should make so much sense right so that's one thing now here's the cool thing usually these stretch receptors are coupled with a specific nerve you know what that nerve is this nerve here this red nerve this right here is cranial nerve 10 wait that's the vagus nerve but here's the cool thing this right here this nerve is the afferent fibers this is a sensory nerve so it's sending signals to the central nervous system while this one is sending messages away from so this is a efferent signal but here's what's cool about this this is
a vago vagal reflex so now another really cool thing is is this information this is called a long reflex arc right so going all the way up vagus nerve coming all the way down vagus nerve that's that's a long reflex arc it doesn't have to be just like that there's also neurons that are actually located in our submucosa if you watched our video on the enteric nervous system you know a little bit more about this we're not going to go into detail of it but there is the special neurons here and it's called the submucosal
plexus and the submucosal plexus can actually stimulate some of these different types of cells parietal cells or maybe even the chief cells and stimulate the hydrochloric acid and the preps in production so again what are these cells right here called this plexus I mean they call this the sub mucosal plexus it also can innovate another one called the my enteric plexus but that's going to be for the contractility of the stomach we're mainly focused on the gastric secretions but do realize that it can also trigger the motility here but this right here look it didn't
go very far that's a short reflex arc so this is a short reflex arc and this is a long reflex arc that's one of the beautiful things here about this mechanism okay so now we know it's coin can be distension activating stretch receptors vago vagal or enteric the next thing is where it gets a little bit cooler okay so now what I want us to do is we have to say there's a specific stimulus but in order for us to understand that we have to come over here for a second in the part of the
stomach specifically called the antrum we talked about that specifically called the antrum there's special special cells these special cells that are located and what's called the gastric glands these specific cells are called entero endocrine G cells but I'm not going to write all that in Tarot endocrine stuff I'm just gonna write G cells entero endocrine G cells they're located in our gastric glands which we'll talk about a little bit later so now these G cells what's so cool about them is they can respond to partially digested proteins okay so let's say here this little orange
guy right here is a partially digested protein if these proteins stimulate the G cells they can stimulate the G cells and let the G cells know hey there's a lot of proteins there's a lot of proteins located in the actual stomach mucosa we need you to take care of this so what the G cells will do is is the G cells will see create a chemical and this chemical that they secrete is called gastrin gastrin is a hormone so it's going to travel through the blood okay so it's going to travel through the blood when
it travels through the blood it comes to a specific cell in our body and that specific cell that it is going to come to is called the parietal cells so here let's bring this guy up here so here's what we're gonna focus on gastrin gastrin is gonna come up here and we're gonna look and see what he can do so Yashiro is gonna come up here so gastrin has specific receptors that are located on this parietal cell okay let's have the gastrin up here in orange so what gastrin does is we're gonna represent it here
is this blue like ball okay this is gastrin gastrin is gonna bind on two specific receptors on our parietal cells this is called a parietal cell a parietal cell these are really good at not only being able to secrete hydrochloric acid but they make another molecule called intrinsic factor but what happens is gastrin binds on to what's called CC k2 receptors holy sister Kynan type 2 receptors when it does that it activates an intracellular mechanism via GQ which increases calcium levels to activate a special pump on the parietal cell this special pump on the parietal
cell its main function is to push potassium out into the stomach lumen and to bring potassium in what did we just make hydrochloric acid because you'll see later that chlorine will come out later but chlorine is just acting as a spectator ion which means this dissolves in solution but the proton is the thing that we want that's going to make the actual environment really acidic so again what was one of the stimuli here come back over here again we said that if there was some type of situation in the antrum that there was a lot
of it we'll represent it like this again proteins lots of partially digested proteins they'll stimulate what type of cells they'll stimulate the antral inteiro endocrine G cells the G cells will secrete gastric gastrin will move through the blood it'll come up to a varietal cell it'll act on c ck to receptors which is cholecystokinin to receptors because it's a part of that natural peptide family it'll signal an increase in intracellular calcium via the GQ pathway we're not going to go into that which will then stimulate the proton pump to push protons out and by doing
that it's going to concentrate this area with protons which is the component of the hydrochloric acid now in the same way a gastrin also has receptors on this next cell this next cell is called a chief cell so this is called a chief cell now chief cells they can be found pretty much throughout the entire stomach within the body they can be found in the antrum too but what's really cool about these guys is they have vesicles so imagine here I have a vesicle and in that vesicle I'm going to have a whole bunch of
these enzyme molecules that are really really special what gastrin does is he again combined on two receptors but these ones are a little bit different so here here's our little circle molecule here this is our gastrin this time it binds on to what's called C ck1 receptors which again still believed to stimulate an increase in calcium levels which stimulated this vesicle to fuse with the cell membrane if the vesicle fuses with the cell membrane it should make this nice little exocytosis like pocket and then here's all my pepsin molecules or specifically pap sin Oh Jen
molecules what happens is pepsinogen can be converted to another molecule called pepsin its active form this is the active proteolytic enzyme meaning it break down proteins this is the inactive form question is how in the heck do we get pepsinogen to pepsin on the in terminal peptide on it on the n-terminus there's a specific sequence that when in the proper concentration of protons within the proper pH particularly optimally around 1.8 to 3.5 a pH around this area if there's a lot of protons this will stimulate the conversion of pepsinogen into pepsin so it's necessary we
need hydrochloric acid and to activate this enzyme so it's so cool so now what we should have in this area is we should have a lot of pepsin and we should have a lot of hydrochloric acid and what was the initial stimulus for this the initial stimulus for this was partially digested proteins now the reason why it's proteins is because this is actually indirectly related to pH it's directly related to pH now here's why so we can say it's related to here's what I mean proteins are buffers okay so they have different sequences so like
for example if I look at this protein here I kind of string it out a little bit here and here's like again here's my n terminus here's my C terminus there's amino acids that can actually kind of they have negative charges like you know like for example glutamic acid or aspartic acid they can tie up some of those protons and by tying up some of those protons there might have been a lot of protons in the vicinity but if you get a lot of proteins you tie up those protons of what happens to the pH
well the pH was initially low we can initially say that the pH was low which means that there's a lot of protons this is completely the same thing if I get a lot of proteins though if there is a lot of proteins guess what happens having a lot of proteins will then shift the pH to what it'll increase the pH which means that there is less protons here's why this is important for gastrin what was one of the things that gastrin did it made pepsin well pepsin is dependent upon this pH range if you go
greater than 3.5 if you go greater than 3.5 it is going to inhibit the conversion of pepsinogen to pepsin that is why this is so significant so the G cells can pick up protein concentration but technically that protein concentration is related to the concentration of the proton molecules which is related to the pH of the gastric acid so that's a really important point to get there next thing I want you to understand this thing is the same exact point here so if we said that this was an inhibitory situation and cephalic it's gonna be inhibitory
and gastric so I want you to remember that the sympathetic nervous system is going to be the primary inhibitor here because it's going to inhibit the parasympathetic nervous system from stimulating hydrochloric acid release and pepsinogen release and again this could be due to stress anything could be due to depression it could be due to anxiety or it could be due to any type of emotional situation that activates the sympathetic nervous system okay so that covers that part for these two phases but there's one more really strong inhibitor here really really strong inhibitor that we have
to mention here let me put it in purple here and this is going to be a molecule called so mat Statten now somatostatin we have to know what his stimulus is and his stimulus is really really low pH which again the same thing is I can write it as high amounts of protons same thing before I do this though I want to take a little bit of time here to explain what is the mechanism that the parietal cell is undergoing to make the hydrochloric acid because that's necessary we should at least understand that first before
we start talking about the somatostatin so in a parietal cell okay this is a parietal cell that we'll focus on a little bit too this is another parietal cell okay so I'm just taking two parietal cells okay now let's get rid of this nucleus here parietal cells have a whole bunch of different proteins on them but one of the big things about the parietal cells is that they have a lot of a lot of mitochondria a ton of mitochondria and because they have a ton of mitochondria they're going to be pretty oxygen dependent but as
a result of cellular respiration what is something that you get as a result of cellular respiration you get a lot of co2 so one of the molecules that as a result of the Sailor respiration process is co2 if you take co2 and you combine it with water and the presence of an enzyme called carbonic anhydrase so islets see a what do you get h2 co3 now here's where it gets cool h2 co3 disassociate s' into protons and bicarbonate so you get these two molecules here guess where that proton is going right there to that proton
pump so then this proton can get flung out here into the lumen where it needs to help in the digestive process so the next thing is this bicarbonate is really cool because you know we're gonna do with that bicarbonate we're gonna push it out here because out here you're gonna have some blood vessels too so we'll just have a small little tiny blood vessel right here here's a tiny little blood vessel now this is important because if we put bicarbonate into the blood like into the gastric veins that means that the blood that's being drained
from the stomach is actually going to be more alkaline in the blood coming to the stomach than the gastric arteries so this right here where the bicarbonate is coming back through these let's say that this is actually gonna be called this right here we're gonna say this is a gastric vein okay you can ignore the part that it's actually red I just want you to understand that this is a gastric vein the blood that's leaving the stomach is more alkaline than the blood coming to it and this right there where the blood is actually in
the gastric veins and high concentration high amounts of bicarbonate this is referred to as the alkaline tide okay now because we're pushing negative ions out of the cell we have to bring negative ions into the cell so as a result we bring another ion in and that ion is called chloride now the chloride is really cool because what the chlorides gonna do is is that chloride has special channels that it can get pushed out now look what we have here we have hydrogen ions and chloride ions what do you think that makes hydrochloric acid such
a beautiful thing okay but here's the thing this proton when we push it out here we need something that's going to help it so there's another thing that we have to account for on the cell membrane on pretty much every cell in the entire body you have these things called sodium potassium ATPase --is and what they're doing is is they're constantly pumping sodium right they're pumping sodium out of the cell and then they're pumping potassium into the cell approximately three sodium out of the cell and approximately two potassium into the cell now what this is
doing is this is kind of establishing a concentration gradient where there's going to be kind of a lot of sodium out here and very little sodium in here so what happens is we have another mechanism for to prevent excessive protons in because we're producing a lot of protons we don't want this cell to become too acidic so what happens is some of these protons if they become in really really high amounts let's say if there's a lot of protons we can't let them sit in here so what we do is we push some of these
protons out here and as a result we take the sodium that we pushed out and we bring it in and it just keeps getting recycled isn't that a cool thing another thing that we should know here is is that the potassium that we have we're bringing into the cell that potassium is so darn cool because it's helping with this pump too so this potassium right here is being drained out passively but then as a result it's being pumped back in through this proton pump this proton pump right here they call this a proton potassium pump
are just in general the proton pump this is whenever they give drugs like a MEP result a MEP rizal is actually a competitive inhibitor of that protein right there which is going to inhibit gastric acid secretion they use that any like GERD okay gastroesophageal reflux disease okay so that covers that part there now we know how we make hydrochloric acid now here's what we're gonna get to now we got to come back and we gotta say okay let's assume that there is just way too much of this hydrochloric acid out here there is these cells
here okay and they're also located in Antrim you have to remember that I gotta put this down here this is in the Antrim this is a antral G cell and this is going to be an antral D cell okay so if there's a lot of protons we said okay so we said that the stimulus is a high intraluminal which is just saying that there's a lot of protons in the lumen of the stomach there's a lot of protons out here this antral D cell can taste the protons it's a chemoreceptor so it has the ability
to pick up on the concentration of this protons and then as a result it C creates a chemical out into the blood it's also a hormone this is called so mat tow statin so responds to this high proton concentration from here he is going to come out of the blood and act on paracrine meaning nearby cells act on this receptor this is called a somatostatin receptor when it does that it inhibits the G cells from releasing gastrin now you got to go back and say okay what happens if we really if we don't release gastrin
well gastrin was responsible for stimulating pepsin secretion and it was also responsible for stimulating proton secretion that makes so much sense because the stimulus was high proton concentration we just lowered it so that's one cool mechanism there okay now you guys notice here that these G cells and these D cells they have receptors on them that we haven't quite covered yet that is where I want to talk about this vagus nerve a little bit more because the vagus nerve can innervate so many different structures in this area so the vagus nerve can act directly on
the antral D cells and antral G cells so if the vagus nerve secrets acetylcholine that acts on these antral D cells it will cause the it'll inhibit the antral D cells from releasing somatostatin because if you remember acetylcholine was from the parasympathetic nervous system it's being released by all of these fibers here these purple fibers from the vagus nerve and that wants to cause gastric acid secretion so we don't want the somatostatin to inhibit that process so acetylcholine will inhibit the aunt Rodie cells another thing is gastrin gastrin when he's secreted you saw how he
was secreted right here in response to proteins well guess what else he can do he can come over here and he can tell this right here so look now gastrin can inhibit the D cells from releasing somatostatin so that's what's so darn cool here in the same way remember antral G cells we want them to go and actually cause pepsin secretion and hydrochloric acid secretion so this receptor here this must be for acetylcholine too but acetylcholine is gonna want to stimulate this stimulating or result more - and more - and results in more pepsin and
more hydrochloric acid secretion really quickly this is an m3 receptor and this is an m3 receptor and then this receptor here for gastrin on the D cells is a CC k - receptor okay we are so close guys okay next thing here we know what is controlling the antral D cells in the antral G cells next thing I want us to cover is what things are stimulating or inhibiting the parietal cells so now let's go to the next point here there's a bunch of different chemicals let's do the first one which is going to be
somatostatin so somatostatin is going to act right here and somatostatin acts on SST receptors so this is so mat tow statin somatostatin is going to actor AG inhibitory pathway by acting through a G inhibitory pathway it is going to inhibit the proton pumps directly so that's another cool mechanism the next one is this purple one which is acetylcholine acetylcholine has muscarinic type 3 receptors here and when acetylcholine binds here it also is going to stimulate this process because it works DeRay increasing calcium levels increasing calcium levels is going to stimulate the proton pump then we
go to these red guys here in these red guys is another cool chemical that we'll talk about quick which is called histamines histamines acts through what's called h2 receptors and this is a stimulatory one and what it'll do is whack through what's called the g stimulatory pathway and that g stimulatory pathway will also stimulate hydrochloric acid secretion so we have a stimulator here via the gastrin inhibitor somatostatin a stimulator of acetylcholine a stimulator of histamine let's throw another inhibitor on there and this guy right here is going to be prostaglandins specifically pge2 and it binds
on to what's called ep-3 receptors and this acts through the g inhibitory pathway and by acting through an g inhibitory pathway it's going to inhibit the hydrochloric acid production as well same thing with the chief cell let's talk about what things can actually stimulate or inhibit the chief cell gastrin we know is one same thing is going to be we have histamines so histamines also have the ability to act through what's called h2 receptors and this will stimulate via the g stimulatory pathway this will stimulate the increased release of pepsinogen the next one is going
to be acetylcholine which can act through m3 receptors and if acetylcholine acts through this it's going to increase the intracellular concentration of calcium and that will stimulate the pepsinogen secretion and the last one here is going to be another molecule and this is going to be a very interesting that one that we'll talk about in the intestinal phase want you to trust me for right now but this is called si and C you'll know that it's secreted from the S cells in the duodenum in response to very very acidic chyme or fatty chyme and what
it'll do is it'll also stimulate through unknown mechanisms their release of pepsin okay one more thing coming over here we have two more cells this is the significant one so this right here this cell here is called an enteric rama fin like cells so I'm gonna put ECL cell now here's the cool thing about the enteric Ramanathan cells they can be stimulated by other chemicals one of the chemicals is they can be stimulated by acetylcholine so it's going to have M 3 receptors for acetylcholine that's gonna stimulate this cell to release a very special chemical
we'll talk about that in a second another one is it can respond to what's called somato statin I'm gonna put SS T but somatostatin wants to inhibit the release of this chemical that we'll talk about in just a second again and one more this next one here is called gastrin in gastrin will stimulate this EC al cell to release what chemical that chemical that this cell is going to see creat is called histamines and this histamines that are secreted what can they do they can stimulate hydrochloric acid through this indirect mechanism and they can stimulate
pepsinogen secretion through this indirect mechanism and the last thing is remember the somatostatin that's the amount of statin right there doesn't come from the antral D cells it comes from this one which is in the corpus this is again another D cell but this is in the corpus or the body all of this right here the parietal cells the chief cells the decent the ECAC ECL cells all of these cells were talking about specific with the corpus or body of the stomach this can this actual receptor here is a m3 receptor this D cell here
is only specifically sensitive to acetylcholine and again since we've seen it all the time acetylcholine when an axon this m3 receptor of a D cell and inhibits the D cells if it inhibits the D cells it inhibits the release of somatostatin if you inhibit the release of somatostatin you render this EC a ECL cell you prevent it from being inhibited which stimulates the histamine release okay such a beautiful thing one last thing that I want to mention before we finish off here is this acetylcholine that's binding onto the antral G cells it's technically another molecule
we say that this molecule I want to make sure that we actually actually clarify this and revise this it acts the same way but this chemical is called G or P gastrin releasing peptide another name for it is called bomb Beason so I just wanted to modify that right there and just say that again the chemicals that are being released are being released from the vagus nerve but the chemical is called GRP gastrin releasing peptide or bumbie's and which will stimulate the castien release okay that's a finish off really quick we're not going to talk
a lot about it in detail we'll talk about it more in the intestinal phase because that's where it's more relative but this hydrochloric acid this pepsin is so corrosive it could damage our own epithelial cells it could digest the stomach itself what protects us from having that corrosive hydrochloric acid and that proteolytic enzyme pepsin one of the big things and like I said we'll talk about it in another video specifically in the intestinal phase is there's a these actual cells and these cells are mucus cells and there's two main types here one is there is
this thing called foe v Oller cells and these are going to be these green ones here and these blue ones here called mucus neck cells and again over here let's just say this mucus neck cells these guys are secreting a bunch of different molecules that form like this next little mucosal barrier and what's in this mucosal barrier is a bunch of different things one of the big ones is there's like 95% of it is water there's a lot of different electrolytes like sodium and potassium and a whole bunch of other different things another one is
there is a lot of phospholipids but the one that's really really important is mucin proteins these mutant proteins really help to be able to form this thick mucosal barrier and one last thing that is so crucial to what let's put it in red here is we need to have a lot of bicarbonate and technically this bicarbonate ion is a little bit below like closer to the actual apical surface of these cells but I want you to get a point here that this thick thick mucosal barrier here is what protects the corrosive damage that can come
from the hydrochloric acid in the pepsin so this big structure that will talk about more detail in the intestinal phase of gastric secretion is called the mucosal barrier and it prevents corrosive damage by hydrochloric acid and pepsin all right ninja nerds in this video we talked about gastric acid secretion with respect to the cephalic and the gastric phase I hope it all made sense I hope you guys enjoyed it if you guys did please hit that like button comment down the comment section and please subscribe as always an engineers until next time [Music] you [Music]
