all right let's finish up this video on fluid and electrolyte balance so we are going to go to those last four hormones that I mentioned before um that we would talk about so here they are all right so as far as fluid balance is concerned we want to take a look at angiotensin's role so one of the first things that Angiotensin II is going to do um get my pen going here uh is stimulate The Thirst Center oops stimulates the third Center in the hypothalamus that will then cause an increase in blood volume and pressure I'm going to go ahead and put this in again I know we've talked about it already but we'll just put a little bullet right here we're going to put vasoconstriction because this is going to be an immediate effective Angiotensin tube I know that it's job is to increase blood pressure and not fluid balance but I always like to put everything together that um particular things are doing and so this way you can see okay not only are we regulating blood pressure but one of the ways that we're going to regulate blood pressure is by increasing blood volume and how do we do that well by Angiotensin II stimulating the hypothalamus and the third center of the hypothalamus all right then we are going to stimulate the hypothalamus itself not just the thirst Center but the cells within the hypothalamus so the paraventricular nucleus and the supraoptic nucleus Ah that's not it supraoptic nucleus I'm like what is a saw okay so what we want to do so hypothalamus remember we're going to stimulate the posterior pituitary so that we can release ADH or water retention at the distilled convoluted tubule and then the adrenal cortex oh that's right there is going to release aldosterone and that's going to be sodium retention and of course sodium retention then is going to lead to water follows salt all right so if we go to the next slide we can look at its effect here so what is the stimulus low blood pressure right there detected by the juxtaglomerular apparatus and then sympathetic division is going to stimulate the um the JG cells to release renin and so juxtapemerial apparatus responds to stimuli so the cells that are around the uh the anterior no the afferent arterial like anterior that's not a thing um and then the JG Jeff JG apparatus releases renin as it says right there we'll just put renin okay so what's going to happen this liver continuously continuously releases engine oh oh my goodness angiotensinogen which is the inactive hormone because anytime you see ojin on the end it's going to be the former of the word thing that's going to form the front of the word so angiotensinogen is going to form Angiotensin but that Angiotensin needs to be um activated by renin that's one but notice that it says Angiotensin one is inactive because it is not completely finished you have to go to Angiotensin II which is the active hormone so uh renin released by the juxical murielar cells is going to as it says in Step number four Ren converts angiotensinogen to Angiotensin 1 and Angiotensin converting enzyme or Ace converts Angiotensin 1 to Angiotensin II when you get into pharmacology and when you get into the nursing program if that's what you're after you will talk at length about this mechanism and Angiotensin converting enzyme and how we can use that to lower how we can inhibit that to lower blood pressure and so just know these are never going away you are going to see them over and over and over again all right so Ace released by the endothelial lining but primarily we see it released in the lungs as the blood passes through the lungs all right so here are the effects of Angiotensin II vasoconstriction increases peripheral resistance and increases blood pressure decreased glomerular filtration rate decreases urine output because if we to maintain blood volume and blood pressure because if we are in a low blood pressure situation remember this is the stimulus we've got to remember renin Angiotensin system always uh stimulated by low blood pressure okay so typically lower than 80 assistive pressure that's lower than 80 could kick in before that but we know that um from what we learned in the renal portion of the chapter 24. that auto regulatory mechanisms in the kidney so myogenic mechanism and tubular glomerular feedback are going to regulate blood pressure going into the kidney between 80 and 180 millimeters of mercury so salt pressure if we exceed those then we really have to affect systemic circulation and maybe we need to affect systemic circulation just so we can maintain blood pressure to your brain or to your muscles or whatever so we want GFR to drop when we have low blood pressure because you don't want to be urinating out all your water so if your GFR is high glomerular filtrate filtration rate is high you're going to produce produce a lot of urine so let's decrease that and one of the ways let's just put that in here because I don't see it's on here we're going to constrict uh the afferent and efferent arterials therefore less blood is coming in and going out and we're just going to keep that knot filtering your blood um activation of third Center we got that fluid intake occurs increases in blood volume and pressure and then we have a release of ADH from the posterior pituitary and release of aldosterone from the adrenal cortex so those are all of the things that Angiotensin II is going to do do you remember that okay antidiuretic hormone remember is released from the posterior pituitary in response to nerve signals from the hypothalamus synthesized in the hypothalamus stored in the anterior or the posterior pituitary let me just show you that again we did this back in the um endocrine system wow it's really not a nice looking thing so we're just gonna take and make this the anterior pituitary the dental hypothesis remember those cells I'm just going to shade that in because we're not going to use it those cells come from um ectoderm from your throat okay so pharyngeal lining of your throat epithelium but this is going to be nervous tissue so these are going to be cells that originate in the paraventricular nucleus and the supraoptic nucleus of the hypothalamus here's the infundibulum so the neurons are going to pass through the hypophyseal uh hypothalamic first hypothalamic hypophyseal cracked so a tract is a bundle of neurons not in a nerve in the central nervous system not in the peripheral nervous system so here's our tract and so when these cells depolarize for example because the osmal receptors have crenated that we talked about before so here's our low plasma osmo receptors and hypothalamus they will stimulate these cells to depolarize and now they depolarize and as that action potential runs down the axon then out will come ADH okay so it's the same thing as if you're sending out a neurotransmitter it's just where is that chemical going into it's going to go into the bloodstream and since that ADH is going into the bloodstream and not across the synapse then it makes it a hormone okay and then that's going to travel to the posterior pituitary and we'll talk about that I mean it comes from the posteritary going to go to the distal convoluted tubule of the collecting duct and uh of the Nephron and collecting decorative nephron all right so what's going to cause the release of ADH low blood pressure from Angiotensin II which is going to stimulate the hypothalamus receptors um we're going to have critical release if ADH if we have severe blood loss and we're just going to kick out the ADH if the blood osmolarity increases so this is two things low blood pressure and high blood osmolarity again detected by our osmo receptors right there those are going to stimulate uh ADH so this one right here this one is the primary like it says the primary stimulus because you can release ADH without Angiotensin II we're just going to kick more of it in when we are in a low blood pressure situation and um and so then we'll be it will be like a double whammy that we've already maybe detected an increase in plasma osmolarity and so now we've got this blood loss situation with our hypopalemic and so we're going to kick out even more with in response to the presence of 80 or Angiotensin II all right so what are the changes initiated by ADH well they're centering and keep this in mind friends because this is really critical thinking on your part is okay ADH I don't want to urinate water I'm in a low water balance what kinds of things would help me re-establish my fluid balance and if you're losing water you there's only so much you can do with the water you have behind left behind so you got to bring in more so you got to increase your fluid intake and how you're going to increase gluten intake stimulate The Thirst Center so just logically put all of this stuff together these are things that you already know so just put everything all together so we're going to increase blood volume and pressure which is going to decrease osmolarity we're going to increase the water reabsorption in the kidneys so here's what's going to happen we're going to see a picture of this in the next slide so in the um collecting duct is where we see the principal cells and this time I corrected it to make sure principle was spelled correctly um as opposed to out in the other slides with sodium so what we're going to do is stimulate the principal cells of the collecting duct to increase the number of aquaporins so these are specifically water transport proteins now up until this point water has been sufficiently able to pass through the plasma membrane because it's small yeah it's not polar I mean it's not nonpolar but it's small and so water up until this point has always gone by osmosis everywhere it has wanted to go okay so keep that in mind but now we really want to increase the amount of water that we're reabsorbing so we're going to put in these water channels and by putting in the water channels now more water will pass into the cells and more water will then pass into the bloodstream so more reabsorption we'll put that more water reabsorption from the kidney from the filtrate let's just put it's we're taking it out of the filtrate all right now decreases fluid loss in the urine absolutely and because we're retaining water we're going to decrease the plasma osmolarity so our our blood fluid our body fluids will allow specifically the blood will be less concentrated and this is important vasoconstriction of the systemic blood vessels which is going to increase peripheral resistance and systemic blood pressure so we're going to use that too the other name of antidiuretic hormone was vasopressin so back in the day uh let me just see specifically when vasopressin was discovered um see and was vasopressin [Music] discovered there we go 1895 wow [Music] usually think of things like in the early 20th century um but yeah we referred to it as Arginine vasopressin which you will still see it called that so ADP Arginine vasopressin um and so Oliver and Schaefer demonstrated that extracts of pituitary altered blood pressure yeah when was vasopressin invented yeah we never invented it probably when life human life was created how about that friend that's when it was invented okay so 1895 that's fabulous so that was the first thing that we found out that it did and then later on we were able to figure out that it also prevents loss of water from your body and then we said well let's call it anti-diuretic hormone as well so I don't think it really cares if I'm talking specifically about vasoconstriction then I'll probably call it vasopressin but typically I'm always typically I'm talking about water balance and I'll talk about I'll call it um antidiuretic hormone all right so here are the stimuli Angiotensin II low blood volume increase plasma osmolarity uh plas the hypothalamus responds to stimulus hypothalamus increases nerve signals opposed to your pituitary to release ADH into the blood uh that's three okay so here is what it's going to do so activation of the third Center we said already go to the hypothalamus okay increase the number of aquaporins so we're gonna put aquaporins here um typically on the um luminal side but it looks like in this picture that they were putting more of them on the basal lateral side but you know what I don't really care I just want you to see here I have these blue aquaporins and what they're going to allow is more water to enter through the collecting duct that go on into the systemic blood vessels or the capillaries in here and then basal constriction so make sure you know all about aquaporins okay all right now what if you don't have so this is too little ADH or if the kidneys cannot respond so you won't retain fluids increase urine production look at that how much fluid do you have in your body as far as your blood so remember you've got nope you don't even have that much three liters of plasma and um 42 so you got 42 liters all together um and then let's see so 42 and two-thirds of that is a number I know this typically let's do it the math okay so 42 times 0.66 okay well it doesn't come out right 42. times 0.66 there we go 27 okay so 27 liters in your cells oh 26 that's the number I normally go with 26 liters in your cells okay and then so 24 that gives you 16 and then 16 minus 3 is 13 liters in your interstitial fluid all right why did I do that not just because I'm wasting time because I want you to see 20 liters of fluid I only have three liters of plasma and I only have 13 liters of interstitial fluid where the heck so I'm at 16 where's the other four liters so that's two two liter bottles that's gonna come out of your cells your cells are going to cremate in this case we can't do that we cannot lose water we can't afford to lose that much water so I had a student that has her husband has diabetes insipidus and so he will drink 24 500 milliliter bottles per day okay so that's he's drinking 12 liters of water on top of anything else that he might consume remember we're only taking in sixteen hundred uh no we're taking more than that 2300 milliliters in food and drink he's taking he's drinking six times more water than we typically take because of his diabetes insipidus because of his lack of ADH production all right now let me just tell you because we're on this so what do you do you get a nasal vasopressin spray and that's typically how we administer it so it can go right into the mucous membranes and into the blood vessels of your nose capillaries in your nose well he's burned out all of his lining in his nose so I can't remember if he was taking something orally um I don't know I can't remember what they're treating him with now but um he couldn't do the spray anymore and uh so yeah it's going to be something that might be with you for the rest of your life all right aldosterone so steroid hormone remember that normally released from the adrenal cortex in response to Angiotensin II decreased blood plasma sodium increase potassium levels okay because remember aldosterone is going to cause you to retain sodium so that's a stimulus for aldosterone release is a decrease in plasma sodium levels if you have hyponatremia let's put hyponatremia and okay and uh we're gonna secrete potassium okay so if we have hyperkalemia then we're gonna also release aldosterone again binds the principal cells the kidney we're going to increase the numbers of sodium potassium and sodium channels causing the reabsorption of sodium and water and because water goes follows salt and increase secretion of hydrogen ions to decrease urine output maintain blood osmolarity um so your body is very attuned to how much water you have and how much sodium your sodium receptors and potassium receptors when that all gets back to normal then we stop secreting aldosterone is a negative good old negative feedback negative feedback all right so let's look at its mechanism in this picture so Angiotensin II produces with a decreased blood pressure increased potassium blood levels because remember you can't have potassium and sodium in your bloodstream at the same time if your cells can't take up any more potassium you've got to kick it out and that's what aldosterone is going to do okay so then the adrenal cortex responds to the stimuli adrenal cortex releases aldosterone into the blood now because it's a steroid okay remember that steroid hormones need a carrier protein so they're going to be bound to this carrier protein right here it's our Uber remember I think I said that in a video back in endocrine system um so they have to be shuttled and then when they get to where they need to go then they're going to unbind and then they're going to pass into the principal cells from the bloodstream okay so we're going to increase the sodium potassium pumps here on the basol lateral membrane and we're also going to increase these sodium channels on the other side of the on the luminal side so here we are on the basolateral luminal side so now we're going to pump out the sodium right here we're going to pump it out into the interstitial fluid and then into the cell so that now we will get increased sodium and then because water is going to pass through then we in get increased water and then here is that um kicking out of the potassium and so um uh we also have this right here increased potassium secretion into tubular fluid and then at the same time as K's go out then hydrogen ions go in and says hydrogen is substituted for potassium and conditions of low ph okay all right atrial naturalic peptide we've been over this a couple of times already but here's our last time at ANP so when your Atria are stretching so you have too much congestion in the Atria and what is going to lead to too much uh congestion in the Atria that's going to be um high blood volume okay so if I have too high blood volume or if I have an increased pressure so that I'm getting more venous return back then we'll secrete ANP so eight from the Atria so A and P decreases blood volume and pressure by going to the kidneys and it's also going to go to vascular we're going to put vascular smooth muscle in here so it's going to dilate it's a vasodilator nasodilate systemic blood vessels vasodilate the afferent arterials and the kidney relaxed and sanginal cells so that we get rid of more water so relaxing the mesangial cells if you remember is going to cause is you're going to increase your filtration surface area in the glomerulus surface area in the glomerulus so now we can filter more blood increasing GFR and increasing urine output because what do we want to do we want to get rid of extra water also we're going to inhibit sodium and water reabsorption in the nephron which is also going to increase urine output decreased blood volume decrease blood pressure inhibits the release of Brenin ADH in the action of aldosterone because all of those seek to retain water and increase blood pressure and that is the exact opposite of what you want A and P to do so remember that A and P is the exact opposite to what we want to accomplish with renin ADH and aldosterone all right so what does the stimulus increased blood volume as detected by Stretch receptors the stretch of bare receptors in the Atria Atria respond to the stimuli atrial release A and P to the blood A and P is a protein hormone and therefore does not require a carrier in your bloodstream so then it's going to go into your bloodstream and then it's going to bind to the effectors to cause vasodilation increase GFR increase loss of sodium and water in the urine and decrease release of renin okay so there's that and that's it hey so we are all done that was really nice that it just took a few minutes to um to finish that off so that's it for flu and electrolyte I will be doing one more video on um uh acid-base balance that I will be using this the ABG video that's in there already um because I think it's it's adequate it's decent it's good I don't want to say it's great but because I don't want to you know whatever be humble um okay so that's it and um you're now on to acid-base balance