Gastrointestinal | Gastric Secretion: The Cephalic & Gastric Phase

antral we want them to go and actually cause the

secretion

of pepsin and the

secretion

of hydrochloric acid, so this receptor here must be for acetylcholine as well, but the acetylcholine will want to stimulate this stimulation or result in more, and more, and it will result in more pepsin and more secretion of hydrochloric acid. very 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're very close guys next thing we know what controls the cells Antral D in Antral G cells.

The next thing I want us to cover is what things stimulate or inhibit parietal cells. Now let's move on to the next point. There are a lot of different chemicals here. Let's do the first one that's going to be somatostatin, so somatostatin will act right here and somatostatin will act on the SST receptors, so this is so somatostatin will act on the AG inhibitory pathway by acting through an AG inhibitory pathway. G, it will inhibit proton pumps directly, so that's another cool mechanism, next is this purple one, which is acetylcholine. Acetylcholine has type 3 muscarinic receptors here and when acetylcholine binds here it will also stimulate this process because it works.

DeRay increases calcium levels. Increasing calcium levels will stimulate the proton pump. let's go to these red guys here in these red guys there's another interesting chemical that we'll talk about quickly, which is called histamines. Histamine acts through what is called h2 receptors and this is a stimulant and what it will do is go through what is called. the g stimulatory pathway and that g stimulatory pathway will also stimulate the secretion of hydrochloric acid so we have a stimulator here through the gastrin inhibitor somatostatin an acetylcholine stimulator a histamine stimulator let's add another inhibitor there and this type here will be prostaglandins specifically pge2 and it binds to what are called ep-3 receptors and this acts through the g inhibitory pathway and by acting through a g inhibitory pathway it will inhibit the production of hydrochloric acid and the same with the main cell, let's talk about what things in It can actually stimulate or inhibit the main cellular gastrin.

We know that the same thing will be that we have histamines, so histamines also have the ability to act through what are called h2 receptors and this will stimulate through the g stimulation pathway, this will stimulate increased release. of pepsinogen, the next will be acetylcholine, which can act through the m3 receptors and if acetylcholine acts through these, it will increase the intracellular concentration of calcium and that will stimulate the secretion of pepsinogen and the last here will be another molecule and This goes to be very interesting which we will talk about in the intestinal

phase

. I want you to trust me right now, but this is called si and C.

You know it's secreted by the S cells in the duodenum. response to very, very acidic chyme or fatty chyme and what it will do is also stimulate its release of pepsin through unknown mechanisms. Okay, one more thing, here we have two more cells, this is the important one, so this is here. The cell here is called branch fin type enteric cells, so I'm going to put ECL cells. Now this is the nice thing about Ramanathan enteric cells: they can be stimulated by other chemicals. One of the chemicals is that they can be stimulated by acetylcholine, so they're going to have M 3 receptors for acetylcholine that will stimulate this cell to release a very special chemical that we'll talk about in a second.

Another is that it may respond to what is called statin somato. I'm going to put SST in, but somatostatin wants to inhibit the The release of this chemical that we'll talk about in just a second again and one more, the next one here, is called gastrin. Gastrin will stimulate this EC cell to release the chemical that this cell is going to create. It's called histamines. And these 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 to remember somatostatin, which is the amount of statin that is there, it does not come from the antral D cells it comes from this one that is in the body this is again another D cell but this is in the body or the body all of this right here the parietal cells the principal cells the decent ones the ECAC ECL cells all these cells were talking about specific with the body or body of the stomach, this may be this actual receptor here is an m3 receptor this D cell here is only specifically sensitive to acetylcholine and again, as we've seen all the time, acetylcholine when an axon this m3 receptor of a D cell and it inhibits the cells D if it inhibits the D cells, it inhibits the release of somatostatin if it inhibits the release of somatostatin, it turns this EC into an ECL cell, it prevents it from being inhibited, which stimulates the release of histamine, okay, it's such a beautiful thing.

One last thing I want to mention before we wrap up here is that this acetylcholine binds to antral G cells. Technically it is another molecule. We say that this molecule. I want to make sure that we really clear this up and review that it acts the same way. way, but this chemical is called gastrin-releasing peptide G or P, another name is called the Beason pump, so I just wanted to modify that right there and just say that again the chemicals that are released are released from the vagus nerve, but the chemical that is released is released from the vagus nerve.

It is called gastrin-releasing peptide GRP or bumbie and will stimulate the release of castien. Okay, that's a very quick ending. We're not going to talk much about it in detail. We'll talk more about it in the intestinal

phase

because that's where it is. more relative, but this hydrochloric acid, this pepsin is so corrosive that it could damage our own epithelial cells, it could digest the stomach itself, which protects us from having that corrosive hydrochloric acid and that proteolytic enzyme pepsin, one of the important things and, Like I said, we will. talked about it in another video specifically in the intestinal phase, there are these actual cells and these cells are mucosal cells and there are two main types here, one is something called Oller enemy cells and these will be these green ones here. and these blue ones here called mucous neck cells and again here let's say these mucous 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 things. different.

One of the biggest ones is that it's 95% water, there are a lot of different electrolytes like sodium and potassium and a lot of other different things, another is that there are a lot of phospholipids, but the one that's really important is the 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 we're going to put in red here is that 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 understand that this thick, thick mucosal barrier here is what protects the corrosive damage that can come from the hydrochloric acid in pepsin, so this great structure that we'll talk about more A detail in The intestinal phase of

gastric

secretion is called the mucosal barrier and prevents corrosive damage caused by hydrochloric acid and pepsin.

Alright ninja nerds, in this video we talk about

gastric

acid secretion with respect to the

cephalic

and gastric phase. I hope everything is clear. sense, I hope you enjoyed it, if you did, please hit the like button, comment in the comments section and subscribe, as always engineers until next time.