Endocrinology | Antidiuretic Hormone (ADH)

all right news nerds in this video we're going to talk about the antidiuretic hormone so the answer to Redick hormone where is it produced it's actually produced or is actually secreted in the posterior pituitary right because it's actually made by these neurons are located within the hypothalamus put of these neurons here located what are they called I mean these neurons are here actually called the super optic it's actually the nuclear that are located up here the axons are coming down to that tract but the Supra optic nucleus you know nucleus is just a fancy word for saying a group of cell bodies in the CNS central nervous system so this is just a bundle of cell bodies right here right that's the nucleus that's what these are the guys that are actually synthesizing the ADH but then they're storing it down here in these little vesicles in the poster pituitary but then whenever there's some type of stimulus they send these action potentials down and release the anti drydek hormone what are those stimuli okay there's mainly two different stimuli so let's say what are the two stimulus of ADH okay let's break this out let's say one over here one stimulus is actually going to be our blood pressure and I'll explain what I mean by the blood pressure the other stimulus is actually going to be the plasma osmolality okay these are the two stimuli here now what does the blood pressure have to be to be a stainless does it have to be low does it have to be high it actually has to be low so you need to have a low blood pressure in order to have this stimulus how does this actually act as a stimulus you know there's a hormone that's actually being produced whenever there's low BP it's called angiotensin ii okay angiotensin ii and we'll talk about that in the renin-angiotensin system what does the plasma osmolality have to be well usually a blood pressures low usually there's some type of reason that the blood volume is low so that might not be as much water so there's very little water in our blood then the blood is very hypertonic which means has a lot of salty and very little water when something's hypertonic the plasma osmolality is said to be high okay so again what did we say is this person's problem they're most likely having hypertonic blood so their blood is very hypertonic what does that mean when something is hypertonic well it means that most likely your water volume or water volume concentration is low very little water in the blood and it also means that you might have a lot of solutes in the blood okay so a lot of electrolytes and different types of nutrient molecules in the blood right so the water to solu ratio is thrown off where there's very little water and more solutes that's a problem because now ADH has to regulate that so these two are the main stimuli okay so how does it actually do it how does the actual hypothalamus pick up this change in the plasma osmolality I'm glad you asked you see these puppies right there these are the Osmo receptors I love these guys these are the Osmo receptors you want to know why I like them because their names make me feel smart okay you know what they're actually called they call them the organum vascular 'some of lamina terminalis that's one of them the other one is actually called the sub 4 Nick Euler organ and these two guys are picking up this change in the actual blood got the tonicity of the blood the concentration of the blood what is it picking up the water and solutes so if these guys are stimulated by what high flies mozz molality they're going to send signals to this super optic nucleus and stimulate the super optic nucleus to start releasing the anti the retic hormone well how does blood pressure stimulate you know there's receptors for angiotensin ii up here let's say that here's the receptor here look at this receptor here for angiotensin ii and angiotensin ii comes in and look what it does it binds on to this receptor and send signals that stimulate the to relieve to send action potentials down and release the ADH so now what is this ETH going to frickin do alright so you see this cell right here this cell is actually called a principle cell so what does it cool it's called a principle cell you know it's actually located it's located within the collecting duct you know where the collecting duct is located in the kidneys so if I look here what I'm looking at in this structure right here as I'm looking at a part of a nephron so now what's the component of the nephron right here the nephron is actually made up of two chunks here one is this tuft of capillaries called the glomerulus the other chunk of it is this what you see this like little like u-shaped structure here it's kind of wrapping around it's called our it's called a Bowman's capsule so the Bowman's capsule and the glomerulus make up the renal corpuscle okay so that makes up the renal corpuscle this the renal corpuscle the other component of it is actually going to be the kidney tubules what parts so you see this little coiled part right there that's the proximal convoluted tubule you see this loop right here that's the loop of Henle and then if you come over here you see this other cool part there that's the distal convoluted tubule this is what the nephron is but we didn't talk about what we're looking at this is the collecting duct a lot of nephrons empty their actual filtrate into the collecting duct but that's where ADH is focusing so now let's go ahead and zoom in on the collecting duct so what I did is there's a whole bunch of cells that make up the collecting duct I'm zooming in on one cell and saying how ADH is functioning so here on this membrane ADH has a receptor you know another name for ADH it's called vasopressin so a vasopressin has receptors located here if we were to be specific this is actually a vasopressin type 2 receptor okay so this is a vasotec basal press and type 2 receptor ADH comes in and look what he does he binds on to this receptor and triggers an intracellular cascade how did he do that so the first thing he does is activates what's called a g-protein so he actually activates AG stimulatory protein and this G stimulatory protein is normally normally it's actually bound to GDP which keeps it off but then what happens is it's going to get bound to gtp which turns it on all right it gets turned on from that right so then what happens he starts moving along the membrane and he activates another enzyme look at this this this is a big enzyme look at this enzyme right here this enzyme right here is called adenylate cyclase and what that G stimulatory protein does is he binds into this adenylate cyclase and activates this adenylate cyclase when he activates the adenylate cyclase what he does is cleaves off a phosphate and turns him back into gdp which turns the g stimulatory protein off but then he's not done he sees ATP and he takes that ATP and converts that into cyclic a and P this is our second messenger what a cyclic AMP II do cyclic AMP II activates a very important protein here and this protein is called protein kinase a so this is an extremely important protein because this protein is going to regulate a lot of activities inside of this cell you know another signal that ADH gives but this G stimulatory protein it also activates these protein kinases and activates two pathways so let's see these two pathways one of the pathways here let's add all the nucleus of this cell and here's the DNA inside of the nucleus protein kinase is actually going to come over here and it's going to stimulate specific genes and the genes are on there going to undergo transcription and translation they're going to make some specific proteins that go to the rough endoplasmic reticulum and then into the golgi and get packed into vesicles so let's draw these vesicles here now let's say here's a vesicle it's actually draw it in black okay here's our vesicle and on this vesicle some very important proteins let's draw these proteins here look at this one right here these proteins right here is actually going to be aquaporins so what do these proteins are called again these orange proteins they're called aquaporins but I'm going to be very specific and I'm going to give these aquaporins a specimen more specific name you know what these are called these are actually called those orange proteins are called aquaporin - they're actually called aqua poor in type - okay why am i mentioning that why am i being so picky well the reason why I'm being very very picky is because there's also aquaporins over here on the basolateral membrane they're all over the place and these these proteins are always open what are these black proteins that I'm drawing now these are also aqua points but you know what type of aquaporins those are these aquaporins are aquaporin 3 & 4 so these black proteins that are located on the basolateral membrane and are always open are called aquaporin 3 & 4 so these ones right there are called aquaporin 3 & 4 and so these were the black channels these orange channels here are going to be the aquaporin - that's why I'm being very specific because these channels are not here when ADH isn't there these channels are only made with ADH is present so normally guess what's running through here anyway we're making urine and our kidneys right so water is actually a very integral component of our urine water is actually flowing through here and if there's no channels they can't get taken in it gets urinated out but you know what else protein kinase a does he's not done there look what else he does he also stimulates like phosphorylation reactions because you know it's what kinase ins knew they put phosphates onto things so like for example pyroshow here it might phosphorylate some transcription factor or it might phosphorylate certain proteins that migrate this guy towards the cell membrane and look it fuses so now this protein is going to fuse with the cell membrane so let's show that so now let's actually show this guy fusing with the cell membrane what is it going to look like now so now look at this let's draw this part here and let's draw all these orange proteins into the membrane let's draw one aquaporin to another aquaporin - and another aquaporin - okay and then again they're merged with the membrane right so this was the part of the vesicle it fuses with the membrane and now the water was just going to get lost into the urine but look what look what happens with these aquaporins because what the protein kinase they do he stimulated the migration of these octopod tubes into the membrane now look this water's flowing by but then these aquaporins open up waters like oh sweet I'm getting in whoop whoop whoop and he runs right into the cell so he gets taken out of the filtrate that we're going to usually hearing it out he brings it into the cell and then guess what else he does with it he's like okay now I can actually move from the cell into the blood because there's not as much water in the blood so now this water that was brought into the cell through these aquaporin twos are actually going to rush out of this cell and when they rush out of the cell they move into the blood so now water is out here in the blood what happens to the plasma volume it increases so now the actual plasma volume goes up if the plasma volume goes up guess what else goes up the blood pressure and if the blood pressure goes up what was the original what was one of the stimuli low BP what do we do we brought it up so we took care of that issue what was the other problem the other problem was that we didn't have enough water in the blood to contribute to the plasma osmolality there was more solutes than there was water so it's hypertonic when we bring this water into the blood our ratio between the water and the salt are going to be close to equal you know what it's called whenever your salt and your water pretty close to equal so then look what happens to the plasma osmolality it was up but now the plasma osmolality is going to go down plasma osmolality Osmo Latif goes down but it tries to approach a point of what's called ISO tonicity so it tries to become isotonic okay you want in other words you want the actual water in the blood to be almost equal to the salt it's about 300 milliosmoles per liter that's about the tonicity of what you want it to be but we took care of the issue didn't we our plasma osmolality is back down our blood pressure's back up we fixed the issue but ADH says I can also do something else you know he also has receptors on blood vessels when there's really really high eighty concentration you know let's say there's actually some smooth muscle cells over here and there's a receptor right here for the ADH on those smooth muscle cells and what happens is in any systemic blood vessel it could be any systemic blood vessel this ADH has another different type of receptor remember you can also call it vasopressin the ones in the kidney were vaso pressing on type 2 this is vasopressin type 1 receptor and then what happens what do we say the ADH can do you can bind on to this actual basal press and receptor and he activates a specific mechanism of GQ mechanism where you increases the calcium in those muscle cells and causes them to contract if you contract the blood vessel used to decrease its diameter so it's called vasoconstriction right so what's the overall result out of this the overall result of this is vaso constriction and what does vasoconstriction do remember decreases the actual diameter so it increases peripheral resistance and what happens if you increase your peripheral resistance you increase your blood pressure okay so that's another way that ADH can try to take care of this issue okay real quick to end off this video let's say what happens just real quickly what happens if we make too much ADH and what happens we make very little ADH so let's say what happens if we start off making very little if you don't make enough ADH so let's say there is a condition in which you don't make enough 88 you want to write this one down it's all so very little so we'll say low ADH hypo secretion usually this is due to like some type of trauma to the head this condition is called diabetes insipidus and again it's usually due to some type of severe like hit or trauma to the head that damages certain areas inside the hypothalamus and the poster pituitary and it can't release ADH if you can't release ath what's the job of ADH to bring water into the blood if you can't do that what's going to happen the water is going to get lost into the urine you're going to be peeing like a mofo all right and when you're peeing so much what's that call when you pee a lot called polyuria and if you have polyuria you urinate a lot if you start your lean urinating a lot you get really really thirsty that's called polydipsia that's one way to determine if someone has diabetes insipidus you actually taste their urine you know back in the day they used to do that they used to drink the urine to see if the urine was actually like sugary to determine if it was diabetes mellitus or if it was really really bitter and watery that could be diabetes insipidus right that's not easy to do back in the day thank goodness we have other tests now all right what happens if you actually make too much ADH so maybe there's a tumor maybe you have some type of tumor in the hypothalamus or tumor here in the posterior pituitary or maybe you were exposed to some type of bacteria that caused meningitis and it start damaging certain tissues and also can lead to ADH secretion whatever it might be you're making too much ADH what do we say ADH does when it's present it brings water out of the kidneys and into the actual blood if you're doing that excessively you're going to hold on to a lot of water you can get puffy all right you don't want that what's that condition called it's called syndrome of inappropriate ADH secretion why is that very dangerous if you bring so much water into the blood what's going to happen to the ratio between your water and your solutes your water is going to be greater than your solutes then what happens is is if you start overpowering the amount of solutes you have in the blood specifically sodium and chlorine that water whatever there's less salt water starts leaking out of our blood vessels because there's not a salt to hold it inside of the blood when it starts leaking out of the blood it starts getting leaked into our brain and you can cause cerebral edema and that's very dangerous right so that's one condition that you have to be able to fix so usually if they have cerebral edema you can give them some type of mannitol to pull some of that water out of the brain but it's extremely dangerous so syndrome of an appropriate ADH secretion is a very severe condition in which you produce too much ADH all right all right engineers I hope all of this made sense I hope you guys enjoyed it until next time engineers

Channel: Ninja Nerd

Views: 180,177

Rating: 4.9667344 out of 5

Keywords: ADH, vasopressin, SIADH, diabetes insipidus, syndrome of inappropriate antidiuretic hormone, antidiuretic hormone

Id: HL89x3BTnmY

Length: 17min 59sec (1079 seconds)

Published: Tue May 02 2017