Endocrinology | Adrenal Gland: Aldosterone

sorry engineers in this video we're going to talk about the adrenal gland alright so first off here where would you actually find the adrenal gland so you know okay if we're taking here anatomical position all right you have your abdominal cavity right now in the abdominal cavity you have your liver on your right side you get your spleen on your left side generally unless you have situs inversus totalis but normally in every individual you usually has liver on the right side spleen on the left side then what happens is you have two kidneys right or right kidney and a left kidney sitting on top of the kidneys is actually going to be your adrenal glands you know another name form is because they're sitting on top of the kidneys is the suprarenal glands okay so you have two of those and they're generally kind of like a pyramid shaped gland alright so if we look here at the adrenal gland we're going to have a couple different layers of it okay well first off there's three layers that make up the cortex let's go over those layers first so you see this orange layer right there that orange layer is the one that we're going to be talking about in this video that is actually going to be the zona glomerulosa and we'll talk about what he's actually secreting in a second this green layer here which is the biggest portion of the adrenal cortex is actually going to be specifically the zona fasciculata and then this purple layer here is going to be the zona reticularis so that purple layer right there is the zona reticularis these three layers make up the adrenal cortex in the middle all you see is a whole bunch of neural tissue now these three are actually more of like a glandular cuboidal epithelial tissue all right this one here in the middle or the medulla the adrenal medulla is a neural tissue so this black component there is actually going to be the adrenal medulla and again all these three components make up the adrenal cortex all right now that we know that we're going to focus on each single one of these layers in an individual video so in this video we're going to specifically focus on the zona glomerulosa ok so what I did here is I zoomed in on his own zona glomerulosa cell and we're going to look at what types of chemicals this zona glomerulosa cell is making and secreting and then what type of target or gets a target organs it's affecting alright so if you look here we have a zona glomerulosa cell right and it has a bunch of receptors here on the cell membrane what are those four because you know this cell doesn't just produce hormone on its own as every cell has to have a stimulus so this has three different stimuli each one varies in significance all right so this first one here this first one here is the most powerful stimulus of aldosterone that's the core moan that we're going to produce from the cell okay so let's see what's happening here with this receptor we'll talk about this this path I'm about to talk about here in a second in more detail in the renin-angiotensin pathway but right now usually I'd Ostrom which is the hormone we're going to talk about is stimulated to be released in low blood pressure so whenever there's low blood pressure your kidneys produce a chemical called renin right so there's specific cells in this kidney called the JG cells juxtaglomerular cells they secrete renin then what happens is random kind of like a little enzyme okay the liver produces a plasma protein this plasma protein that the liver is actually producing is called angiotensinogen what renin does is renin acts on the angiotensinogen so imagine here I have little scissors the renin is the scissors it's going to cut a specific portion of the angiotensinogen and convert this into angiotensin one okay so now angiotensinogen is getting acted on by Renan okay and then Renan converts angiotensinogen to angiotensin one there's another enzyme here in the lungs in the lungs there's an enzyme over here and this enzyme is actually called angiotensin converting enzyme ace and look what it does it converts angiotensin 1 into angiotensin 2 okay and this is that enzyme this enzyme is doing that he's stimulating this conversion so Renan stimulates angiotensinogen to turn into angiotensin one and then angiotensin converting enzyme in the lungs turns to angiotensin 1 and to angiotensin 2 so angiotensin 2 is going to come over here to the zona glomerulosa of the adrenal cortex and stimulate the production of aldosterone we'll see how so now let's follow this angiotensin 2 he comes over here and he binds on to this receptor this receptor is a g-protein coupled receptor so you know what proteins can activate it's going to activate G stimulatory protein and if you guys are watching these videos you know that G stimulatory protein is normally bound to gdp but when this angiotensin 2 acts on the receptor it gets rid of the GDP and puts on gtp which turns the G stimulatory protein on once this G stimulatory protein is on it activates a effector enzyme here in the cell membrane that affect your enzyme that's actually going to be sitting here in the cell membrane right this enzyme here he's always glad to help this enzyme is called adenylate cyclase and what that does is that converts ATP into cyclic a and P and then cyclic AMP is then converted activates activates protein kinase a ok why is that relevant we'll talk about it in a second ok well we're going to put this together let's just wait another thing you know your hypothalamus is usually releasing specific types of chemicals in response to hypoglycemia response to fever or other different types of stimuli you know what that are stress this chemical that it's actually secreting is called corticotropin-releasing hormone so what chemical is it secreting it's secreting what's called corticotropin-releasing hormone corticotropin-releasing hormone comes over here and acts on this specific cell by the way what nuclei are releasing is corticotropin-releasing hormone this is going to be by the para ventricular nucleus right which is in the hypothalamus because this is the hypothalamus mammillary bodies infundibulum poster pituitary and pituitary right CRH acts on these cortical tropes and stimulates these cortical tropes to start producing a hormone called adrenocorticotropic hormone and then the adrenocorticotropic hormone goes to the adrenal cortex now adrenocorticotropic hormone is not one of the most strongest stimulus if anything it's actually one of the weakest stimuli of the zona glomerulosa so now look comes over here and he binds on to this receptor and again who is this adrenal cortical trophic hormone now adrenocorticotropic hormone is a stimulator just like angiotensin ii is a stimulator but this is a very weak stimulator but nonetheless same pathway so what would it do is activate a G stimulatory protein binds to gtp you guys already know this story activates adenylate cyclase and then what does that adenylate cyclase do adenylate cyclase converts ATP into cyclic a and P cyclic AMP e activates protein kinase a okay now it's time I tell you here so you know within the actual zona glomerulosa of the adrenal cortex it's going to have a lot of different types of molecules in here one of the really important ones is called cholesterol cholesterol is very very abundant within these cells because you want to know why the adrenal cortex of the zona glomerulosa and a lot of the adrenal cortex cells are synthesizing steroid hormones not protein almost to this point we have only been dealing with protein or peptide hormone synthesis this is going to be steroid hormone synthesis okay so now the basis of steroid hormone synthesis starts with cholesterol so you have to start here with cholesterol then you know cholesterol is converted into pregnenolone pregnenolone is converted into progesterone progesterone is eventually converted into it's called a leaven deoxy corticosteroid then it's converted into specifically after that it would be converted into corticosteroid and then it's converted into a very important hormone and this is going to be called aldosterone this is the mother of them all okay so now if you look here all of these pathway requires it requires multiple enzymes that we're not really going to be very concerned with one of them is kind of significant and we'll talk about it specifically right here in this step we'll talk about when we talk about hyper or hypo secretions this enzyme is called 21:00 hydroxylase this one we will talk about but it's basically the part of one stimulating and driving this step this is an important step I would actually memorize specifically if you don't remember any of these enzymes I could talk about this is one of them 21 hydroxylase he converts progesterone into eleven deoxy cortical steroid and then there's 11 hydrolysis but then cortical stearin is made into a doctrine why am i mentioning this because before we've only dealt with amino acids making proteins now we're taking cholesterol and taking that cholesterol converting into a steroid hormone okay what's happening with all of this stuff over here I'm glad you asked because guess what these protein kinase aids are doing their phosphorylating specific points within this pathway here so you see how all these pathways are regulated by specific enzymes this protein kinase a is going in phosphorylating multiple enzymes involved in this steps so again what would be happening over here with this guy this guy would be doing the same thing right protein kinase a would be coming over here and what would he be doing he's going to come over and he's going to activate specific enzymes catalyzing these pathways - okay and again activating this pathway or this pathway okay that's all these guys are doing they're just activating these protein these protein kinases are phosphorylating different enzymes of proteins involved within this cholesterol pathway to synthesize aldosterone that's it okay now these are some of the stimuli one more stimuli that's very odd very very different and it's probably one of the second abundant stimuli so this is the first one I would mark this I would actually remember this guys this is the strongest stimulus this is the second strongest this is the weakest stimulus okay we're only talking about stimuli I'm not going to talk about the inhibitory I'll mention at the end but we're going to focus on this first so now what is this actual stimulus this second stimulus this cells very sensitive to the sodium levels and potassium levels in the blood so if our sodium levels in the blood are ever low okay and the potassium levels are high these can exert a specific type of stimulus they can actually flow into the you know they can actually undergo some type of stimulus humoral stimulus and stimulate the production of aldosterone okay so again if there's low sodium levels or if there's high potassium levels what do you call when you have low sodium levels they call it hyponatremia and what do you call whenever you have high potassium levels in the blood they call it hyperkalemia so you know what would this be called if you have low sodium levels in the blood it's called hypo in the tree Nia okay hi sorry low sodium levels and then if you have a lot of potassium in the blood this is called hyper kalenna which is extremely dangerous both of these are very dangerous if this was imbalanced but these are stimuli about Bostrom let's talk about one more okay we talked about a lot of stimuli let's talk about an inhibitor on this actual membrane you have another receptor here okay you know the niches for atrial natriuretic peptide he secreted whenever your blood pressure is really high but guess what he's going to do he's not going to activate a G stimulatory pathway he's going to activate a G inhibitory pathway and what's the overall result of a G inhibitory pathway it'll result in potassium efflux out of the cell and if potassium is leaving the cell what's the overall result of potassium is leaving the cell if potassium is leaving the cell this is going to cause hyper polarization and this hyperpolarization could alter some of the enzymatic activity within this cholesterol pathway but overall results here is that this is an inhibitory effect of aldosterone synthesis so let's clear this then angiotensin 2 is the primary stimulus of aldosterone secretion hyponatremia and hyperkalemia is the second strongest stimulus of aldosterone secretion and then the last one was adrenocorticotropic hormone is the weakest stimulus of aldosterone secretion but then what was the inhibitor what was the very very powerful inhibitor of aldosterone secretion this is going to be atrial natriuretic peptide it works through a gene hibbott or e pathway and causes potassium ions to leave hyperpolarizing the cell which alters the enzymes within this pathway and the overall result is inhibiting aldosterone synthesis okay now that we know that we know how we've made a - - and I'm only telling you guys is because it's important that you understand the difference we went over protein synthesis we have to understand cholesterol synthesis okay our by a steroid steroid synthesis of these hormones based on cholesterol okay now that our - runs made let's go ahead and follow him to his target organ so look what he's going to do he's going to circulate out here and he's going to move in the blood right now generally adoptions of steroid hormones so you usually want to have him bound to certain types of proteins here in the blood stream usually the protein he's usually bound to in the blood stream is actually called trans Courtin so he can actually be bound to trans Courtin which is another word for corticosteroid binding globulin so I'm going to put corticosteroid binding globulin and who combine their aldosterone and he can also bind on to another protein that you guys are probably familiar with called albumin so he can also be bound to albumin the whole point here is that he can't circulate in the blood on his own okay he has to be bound to a protein transport protein then where is he going he's going to go and act on this specific cell here this is his destination where is this cell located well if you look here you guys are probably seen this diagram a couple times we're looking at a component of the that front right so nephron is consisting of a glomerulus and the Bowman's capsule proximal convoluted tubule loop of Henle and distal convoluted tubule right and this is in the kidneys so this is in our kidneys and specifically he's going to be focusing on the cells of the distal convoluted tubules so what portion is he looking at here he's mainly focusing on the distal convoluted tubule and what's his effects let's see here he's a steroid hormone right so steroid hormones they actually can pass right through the lipid bilayer looks what it look what it does it comes over here and it binds on to this receptor this nuclear or intra cytosolic receptor basically a receptor inside the cell for the steroid hormones lipid-soluble once it binds onto and again who is this molecule here who is this blue molecule I should write this right so this is going to be aldosterone just so that we know you keep track of them right when this binds on to this receptor this receptor becomes active and he comes over here and stimulates a specific gene sequence actually he activates a couple different genes okay so he activates a couple different genes what are these genes that he's going to do what's what's going to happen to these genes these genes are going to undergo transcription so right you know from DNA if you make RNA this is called transcription so it's going to make specific types of mRNA and then that mRNA will undergo translation to make specific types of proteins what are these proteins look at what happens here he plugs these beautiful blue proteins into the membrane okay so let's draw one more beautiful blue protein here and then he plugs in these black proteins into the membrane okay and then he also helps to put other proteins around the membrane let's draw these proteins over here let's say he also makes these proteins okay so now the we've talked about that he's activated three genes to make three different types of proteins what are these proteins that have been synthesized so this protein over here you already know what this guy does we've already talked about this guy before watch what's going to happen here I'm taking three sodium pumping it out taking two potassium pumping it in taking what am i doing over here I'm taking the three sodium pumping it out taking two potassium pumping it in and what is happening within this you're directly utilizing ATP so this is utilizing 80p okay that's one thing he's increasing the expression of these proteins to develop a concentration gradient what else is he doing that's one protein that he synthesized he also is making these proteins guess what these proteins are for you know who's flowing through this area sodium sodium is kind of floating through this area right now now generally this distal convoluted tubule is impermeable so sodium can't get into this cell normally unless aldosterone is present why because this protein has just been synthesized so now look what happens sodium is going to move into the cell here oh man that's awesome and then what's going to happen that sodium can actually be brought out into the blood or he can either be a part of this whole sodium potassium pump - right so he can also be involved in this - either way what do we do we put a lot of sodium into the blood so now what's happening to the blood levels of sodium sodium in the blood is actually going up what was the original stimulus here low sodium levels what do we just do what do we do we brought the sodium levels up we fix that problem okay what about these black protein channels these black protein channels here are also going to be synthesized but what was the problem before there was a lot of potassium right a lot of potassium in the blood well guess what we're going to do with that potassium we're going to get rid of it we're going to excrete it out and it's going to go out through the urine so what is a Dasha undone he's made three proteins one protein is the sodium potassium pumps to establish a nice gradient for sodium and potassium another thing is you put these protein channels into the luminal membrane for sodium transport from the filtrate into this cell and into the blood and then what happens he gets rid of the potassium and this potassium could be coming from the blood so if the potassium is coming from the blood and being utilized here right so it's being utilized here what's happening to the potassium levels in the blood it's going down because we're getting rid of it okay and that be lost in the urine okay that's that part now another thing if you increase your sodium levels in the blood usually what loves the fall of sodium water so if water is falling so if water is actually following the sodium what happens to the volume of the actual blood because who's following here water loves the fall of sodium so then if the water is actually following the sodium what's the overall result from this if you have more water and more sodium in the blood what's the overall result it increases your blood volume because your salt is going to pour more on water into the blood and then an increase in blood volume increases your blood pressure what was one of the stimuli I told you so if you remember the JG cells releasing renin cleaving angiotensinogen to angiotensin 1 and then converting into angiotensin 2 with the ACE why remember I told you this is because of low blood pressure that was the stimulus for angiotensin 2 now look we brought it back up we fixed the problem so we brought the blood pressure up we brought the sodium levels off we brought the potassium levels down so now you can see why angiotensin 2 is a very powerful stimulator and why sodium potassium is a close second now what about this ANP if a MP is inhibiting this aldosterone from being released what would be the stimulus for a and P high blood pressure okay so whenever there's high blood pressure okay so there's high blood pressure this would be a stimulus of the atrial natriuretic peptide to a and P and if that's a stimulus of a and P a and P is going to inhibit a dosterone why because our dosterone is just going to do what to the blood pressure bring it up so you don't want to release any more l dosterone if your actual blood pressure is already high that should make sense okay ACTH like I told you it's just a wee very weak stimulator it's usually in stressful situations so usually this is occurring more end stress this has more of an effect on me zona fasciculata in the zona reticularis which we'll talk about but very little effect on the zona glomerulosa but it does have a very very weak stimulus and it can stimulate a little bit about dosterone secretion okay so in this we've talked a lot about our dosterone I hope all of this made sense I really hope you guys enjoyed it in the next video we're going to talk about the zona fasciculata with respect to cortisol alright engineers until next time

Channel: Ninja Nerd

Views: 374,316

Keywords: adrenal gland, zona glomerulosa, suprarenal gland, endocrinology

Id: HZhz-7Grux0

Length: 25min 0sec (1500 seconds)

Published: Thu May 11 2017