RENIN-ANGIOTENSIN-ALDOSTERONE REFLEX by Professor Fink.wmv

the last hormone that we're going to cover to show off our presentation of hormones before we move on to cardiovascular physiology is pictured on 134 G and this is an absolutely unbelievable extraordinary homeostatic reflex your kidney is an endocrine gland I mentioned earlier it appears almost every tissue in the body secretes hormones so probably you never heard this in biology or Anatomy in fact your kidneys secrete more than one hormone the hormone that we're going to talk about that the kidneys secrete is a hormone called remnant it's easy to remember Rendon comes from the kidney because renal means kidney this is called renin later and not today we're going to talk about another hormone produced by your kidney called erythropoietin and if you may have heard of that because it's sold at a brand name called epoch Ritter Epogen we'll deal with that in another time so it secretes more than one morning now there are specific cells in the kidney called juxtaglomerular cells or JG cells they're what secrete renin there are three things that trigger these JG cells to start secreting rented into the bloodstream the three things that will cause these cells to release renin is a drop in blood pressure to the kidney a drop in the plasma sodium levels or a rise and increase in the plasma potassium levels that triggers this hormonal on the estatic reflex now remember what a homeostatic reflex is for the purpose of a homeostatic reflex is to compensate or correct for stress for a problem if you're too hot the homeostatic reflex is you sweat to cool yourself down if you won't walk into a dark room the homeostatic reflex is your pupils dilate to take it more light if your blood sugar level is too low the obviou static flex is to release those hormones that raise your blood sugar level that's always when homeostasis is about so if this is going if these three things are going to initiate on the estatic reflex the whole purpose of the reflex is it's going to compensate or correct for all three of these problems thinking about this this makes this a very very important reflex because this is a reflex that affects in part your blood pressure and it controls the two most important minerals or electrolytes in your body sodium and potassium now what is renin do renin is released into the bloodstream and it acts on a protein circulating in your bloodstream there is a protein always in your bloodstream caught angiotensinogen now we where have we previously learned that most plasma proteins are made in the liver so the liver makes all kinds of different proteins the main one it produces is a protein called albumin but it produces many many other proteins including a protein called angiotensinogen now this is always circulating in the blood stream renin activates it it activates it and turns it into something called angiotensin one now I might just mention that there are many proteins that have to be actually quote activated and if a protein does have to be activated the inactive form usually has the ending GE and Jim and so then when it becomes activated you basically just drop that g en ending so it goes from angiotensin Ojin to just angiotensin there's a we're going to learn other examples of this I'll tell you two other examples you maybe you've heard of them maybe you have your stomach cells secrete an inactive enzyme called pepsin ojen and the hydrochloric acid activates it pepsin all right so it goes from pepsinogen to pepsin later we're going to be learning in hematology about a blood clotting protein in our blood stream called fibrinogen that is turned into fibrin so these are just examples of what I'm saying now how does it activated I this upper diagram you have to know right below though you don't have to know this but I'm just explaining it angiotensinogen is a protein a polypeptide and this is the sequence of amino acids that make up at angiotensinogen you'll notice it shows you you don't have to know this ribbon Cleaves or splits off four of those amino acids so by cleaving or splitting off these four amino acids that turns it in changes it from angiotensinogen to what's called angiotensin one that's how it's quote activating it it's actually made it shorter now we're not done yet in activating it there is an enzyme in your lungs I mean this is the story you would it's hard to believe this is real there's an enzyme in your lungs called AC E which stands for angiotensin converting enzyme as the angiotensin one is carried in the bloodstream through the lungs this enzyme in your lungs converts angiotensin 1 into angiotensin 2 now again I want you to know that but I'll just show you you don't have to know this but I'll just show you what that means here this was angiotensin 1 what does this angiotensin converting enzyme or AC e do what does it do it splits off another 2 amino acids off that angiotensin one turning it into an even shorter polypeptide chain code ang - so it's been cleaved or split twice now okay again you don't have to know that I'm just trying to explain activation now angiotensin ii is sakura is now in the bloodstream it was converted from one to two and it circulates in the bloodstream and it specifically activates the adrenal cortex to secrete aldosterone and other mineralocorticoid steroids now we have previously told you that the adrenal cortex actually secretes three different types of steroid hormones adrenal androgen glucocorticoids like cortisol and mineral corticosteroids like aldosterone we last class meeting we learned that what controls the release of cortisol another and other glucocorticoid steroids was the pituitary hormone ACTH adrenocorticotropic hormone but what's controlling the release of the aldosterone and other mineralocorticoid steroids is this renin-angiotensin mechanism so this is controlled by totally different mechanism than what controls the release of cortisol now aldosterone is secreted into the bloodstream by the adrenal cortex and it affects the kidneys and what does it cause the kidneys to do it causes the kidneys to do three things number one and I'm going to start with number three here one of the things that the aldosterone causes the kidneys to do is to increase potassium excretion it causes the potassium and the bloodstream to be excreted out of the bloodstream into the urine so what is it doing to the amount of potassium in your blood it's lowering it it's causing the potassium in your blood to be X screening to eliminate to get it out in your urine to get it out of your body so can everybody see then that that compensates for when your blood potassium levels too high when your blood potassium levels too high this wreden angiotensin aldosterone reflex causes your kidneys to excrete that excess potassium this is why as we learned a long time ago there is not a warning label on every Chiquita banana not to exceed three bananas because if you had we're in the mood for having a banana split or a banana milkshake I guess you can even make a banana daiquiri alright another strawberry daiquiris but okay the am so I don't sort of thinking about something alcoholic thing but then yeah you got you're in the mood for four bananas and you go bananas are high in potassium and as you eat them you're going to raise your potassium levels so why don't you have to worry about developing hyperkalemia the answer is because if this whole only ostatic reflex is working right it's fine there's not a problem there's no problem with you drinking extra water because you'll pee out the extra water there's no problem and going into a cold room because you'll do your body will respond to warm you up so this is called homeostasis this allows us to deal with life so that compensates right for this now another thing that the aldosterone causes the kidneys to do is to increase salt retention it causes your kidneys to retain salt this is the compensation for low sodium levels so if your salt or sodium levels were low instead of your kidneys peeing out that salt you retain it alright so if you don't want to get rid of the sodium or salt cause you're low in it so that compensates for having low sodium levels in your blood those are the two most important minerals or electrolytes in your body so this is the mechanism that controls it now we also said that a drop in blood pressure would trigger this reflex the aldosterone causes your kidneys not only to retain salt but also water and by increasing salt and water retention and at this moment some of you might be thinking is this like eh I'm going to compare and contrast this with ADH in a moment this is not like ADH antidiuretic hormone cause your kidneys to retain only water and the purpose of retaining water was if you're too salty you detained water to dilute that salt and bring you back down to being isotonic here you're retaining both salt and water you're actually retaining isotonic fluid not water but isotonic salt and water the purpose of this is to expand your blood volume by expanding your plasma or blood volume that raises your blood pressure and of course if this is raising your blood pressure you can see that compensates for the fact that what initiated this reflex was included a drop in blood pressure now if you're having trouble imagining how increasing salt and water retention which increase it in your blood which increases your blood volume which causes your blood pressure to rise if you're having trouble in that intuitively getting feeling this sense that if your the amount of blood in your vessels it becomes more than normal or at least let's say it becomes bit more in your vessels that increases the pressure in your vessels in fact if you're having trouble understanding that consider the opposite if you were bleeding if you had cut yourself and blood is going out of your blood vessels what's happening to your blood pressure it's dropping I think everybody gets that one if the blood if you lose blood out of your body as the blood volume drops your blood pressure drops well if the drug lowering blood volume lowers your blood pressure increasing your blood volume raises the blood pressure so that's that how that's how it's compensating now this whole mechanism is almost really beyond belief frankly you might remember how I had proposed that if I had been on the design team for designing a human body remember how I proposed eliminating the lymphatic system simply by making the colloid osmotic pressure and the blood equal to the blood pressure so they would balance each other out so we wouldn't need a whole additional another system of vessels I have another suggestion if I have been on this design team you'll notice that what triggered this whole reflex was a drop in blood pressure a drop in sodium levels a rise in potassium caused the kidneys to release renin rendon activates angiotensinogen to angiotensin one this enzyme in the lung converts angiotensin one in angiotensin ii which causes the adrenal cortex to release aldosterone and what does aldosterone do it comes right back to the damn kidney again and causes the kidney to make these changes you know I would have said let's let you know we can pet out all this if these three things happen just make your kidneys do those three things if these things happen you know what let's skip all that let's make your kidneys just do those three things and that compensates so if I've been on the design team I could have eliminated most of us but nobody cared what I thought so instead it's got to go through this entire bizarre loop of things to come right back to the kidney where a beginning I don't know why it's what's just that just as the long as it takes to go from one hormone to the next so again it's always slower than the nervous system works but it's a matter of hours so anyhow so that's the mechanism let's on the previous page I'm sorry on the next page 134 H backslide so I want to summarize what we just said and in the process I want you contrast the renin-angiotensin-aldosterone homeostatic reflex with ADH antidiuretic hormone and I'm doing this because this is commonly where students feel they they get a mixed up because then they're asking what's the difference between now it's interesting that the aldosterone is the last hormone that I'm presenting right now and ADH was the very first hormone I presented so of ADH antidiuretic hormone where did it come from you remember that it was produced by hypothalamic neurons that released it from the neural hypothesis what did now what triggered the release of ADH you know from the neuro hypothesis an increase in tonicity saltiness of the body fluids especially the cerebrospinal fluid we had said that if you ate a lot of salt it's salted pistachios salted popcorn pickles you get the idea salted potato chips you absorb the salt now you're hypertonic so that's not good we don't want your extracellular fluids to be high bora hypertonic we want them to be isotonic so that the cells won't shrivel up or swell up so that triggers the release of a th you become thirsty to drink more water and ath what is abh do ADH causes your kidneys to retain water and only one now where you'll notice that I did indicate that a drop in blood pressure will also trigger ADH release but I'm not going to test you on that I put it in parenthesis I won't test you on it yes your book mentions it everything in the body is multifactorial there's always a multiplicity of things I've also we're going to ignore this part right here because we haven't gotten the kidneys so exactly how the details of how ADH works that deals with the details of the kidney but what is the basic function of antidiuretic hormone and is called an antidiuretic means it means it stops you from peeing you retain water the purpose is to increase water retention to retain more water to maintain the tonicity of your body fluids to keep you isotonic when you're too salty or hypertonic it makes your kidneys retain water rather than excreting that water maintain that's its main function to keep your totosai 300-million smolder now right below that the next box the next two boxes indicate the clinical problems of either having too much excess or too little a deficiency and you'll notice what we wrote is there is clinically never been a reported case of anybody over producing ADH who knows what we might find but obviously it hasn't been reported so that's not an issue but there is has been reported clinical cases of where the 80-inch levels have been lower than normal they are deficient and a deficiency of antidiuretic hormone goes by the name diabetes insipidus and so this raises the whole question of what does duck what's diabetes because this is called diabetes insipidus now first off let me just tell you that if you don't make ADH what is abh stand for antidiuretic hormone anti diuretic it stops you from peeing it causes you to retain water so if you can't make this hormone you pee a lot right all you do is pee a lot you pee out a lot of water because you have no way of not peeing a lot of water you don't have this antidiuretic hormone so what does the word diabetes mean the more diabetes means to pee a lot it means to urinate that's what it means it's a Greek word and it means to urinate that's what diabetes means now some of us are getting really confused so I want you to know there are two types of diabetes two very different types of diabetes the diabetes that we have spoken of previously is called diabetes mellitus mellitus is a Greek word just like the word diabetes that means sweet it literally means sweet pea sweet urine the person is peeing a lot and their sugary this type is called diabetes insipidus this is insipid or brackish pee pay the doesn't taste sweet I did say what do you mean taste these two conditions were recognized by the ancient Greeks they didn't have spectrophotometers to measure sugar levels in the blood or the urine when people who peed a lot they would taste their urine and if they tasted sweet they called it sweet pea or diabetes mellitus if they were peeing a lot and it didn't taste sweet they caught it diabetes insipidus so this has been known for quite a long time four people had to peel up now let me just remind you of diabetes mellitus which is the more important problem of the two because that's much fairly common this is rare sweetpea remember we talked about diabetes back in Section B after we dealt with cellular respiration we said that the fundamental problem in diabetes mellitus is you don't have enough insulin so therefore the sugar levels keep getting higher and Aaron higher in your bloodstream because without insulin it doesn't transport the sugar into the cells everybody remember that so it leads to hyperglycemia and the sugar levels get so high in the bloodstream it starts spilling over into the urine so they start getting sugar in their urine remember that so that's called glucose urea why cause URI and we know people have these little dip sticks that can test their urine to see if their sugar there and it should normally not be there because as the sugar starts to spill over from the bloodstream into the urine it osmotically draws water with it it's called an osmotic diuresis when you have all this sugar coming out of the blood into the urine because it's just so high of a level it pulls water with it so people have sugar in their urine also urinate a lot that is one of the classic indications that somebody might have diabetes if you've ever filled out a medical questionnaire one of the questions they ask is frequent are you frequently thirsty and urinate a lot and people who have uncontrolled on manage diabetes have to drink a lot because they pee a lot because of this osmotic diuresis they also of course have the smell of acetone on their breath these are the things you're using to kill you in even before you run the blood tests the smell of acetone on the breath the fact that they report that they're peeing a lot very frequently this is called doing a physical examination a word about medical history a workup of the patient where you're trying to figure out or sort out what's going on in them even before you've got the results of your lab work your lab tests all right now is everybody time reminded you of diabetes mellitus this is diabetes insipidus so in this case the person who has a deficiency who cannot make a th they always pee out a lot of urine because they don't make this count the hormone called anti diuretic hormone that would caused them to retain water so have to drink a lot of water all right now that I've reviewed ADH and also now we understand their diabetes better so let's contrast let's contrast aldosterone with antidiuretic hormone all right so aldosterone is a steroid hormone secreted by the adrenal cortex as far as its factors that lead to the release of it there are three things that trigger ultimately the release of aldosterone that lead to this renin-angiotensin-aldosterone reflex the three things were a drop in blood pressure to the kidneys a drop a lowering of the plasma sodium levels and a row or a rise in the plasma potassium levels any one of these three will trigger this reflex again we haven't covered the kidney so we're not going to deal with the specific physiological mechanism of how it works but the function of the retina offense and aldosterone reflex is to increase salt and water reabsorption or retention notice any H only increased water retention so that's going to affect olicity if you retain both salt water that's not affecting tonicity that's just causing you to retain more salt and water isotonic fluid and also the aldosterone increases potassium excretion the elimination of potassium out of the blood stream into the early so it's job basically is to maintain the blood volume and blood pressure and to maintain plasma sodium and potassium electrolyte levels and just before the break let me just mention these conditions hyperaldosteronism and hypo aldosterone ISM these are not new words the first time we mentioned these were on pages 41 and 42 what were you're dealing with in problems and in fact one of the quote essay questions we you had was we asked you what could lead to hyperkalemia and and many of you wrote kidney failure and what what's the result of hyperkalemia and you wrote depolarization of cells and how would you treat that and many of you wrote diuretics and there's others clever ways so that was hype so let's just review this hyperaldosteronism this is where somebody is over secreting there's an excess aldosterone now what does aldosterone do aldosterone causes you to maintain salt because of the kidneys to retain salt and water and excrete potassium by retaining more salt than normal it creates hypernatremia elevated sodium levels obviously these affecting sodium is always going to affect action potentials it's not a fatal thing but it does affect things by retaining more water as well as salt this increases the blood volume increased blood volume is called hyper volley mia hyper means increased Vall means volume amia means in the blood increased blood volume increasing blood volume we said will raise blood pressure but this if you're producing too much of this aldosterone you're going to raise the blood volume and blood pressure to much more than normal and that's called renal hypertension so you've you've heard the word high blood pressure and then you've heard there's something called renal hypertension this is renal hypertension this is high blood pressure because of hyperaldosteronism causing excessive amounts of salt and water retention leading to high blood pressure increase blood volume and increase blood pressure and another thing that this leads to is that the person excretes excessive amounts of potassium out of their bloodstream leading to hypokalemia now when the potassium levels in the blood and extracellular fluid become lower than normal potassium and the cells start flowing out of the cells and all the cells electrically become more negative than normal or hyperpolarized hyperpolarization of all the cells which we covered back on page 41 and we just be tested on it but in case you've already forgotten hyperpolarization of all the cells causing it causes a slowing down of all electrical activity in the entire body everything's wrong the heart rate slows down electrical activity in the nervous system slows down gi motility slows down everything slows down with hypokalemia remember we said that in an infant who had developed hypokalemia who needs Pedialyte until they get that potassium they're just lying there not moving their heart rates lower than normal they're breathing with great difficulty everything has slowed down abnormally all right so that's hyperaldosteronism now I brought a dustman as it is serious it leads to some serious problems but you don't die from it the wind said that the fourth hormone that was absolutely essential to life was this aldosterone if you have hypo aldosterone Azzam a deficiency you'll be dead why does this result in death so let's again think back what does our doctrine do aldosterone causes the kidneys to retain salt and water and get rid of potassium if you don't have this hormone that means you won't retain salt and your salt or sodium levels would come lower than normal now that's not why you died but obviously that affects action potentials by retaining not only less salt and less water your blood volume drops and if your blood volume drops your blood pressure just the reverse of the oven and this is and when this is called circulatory shock you know back when we were learning about edema and dehydration and how blood pressure could increase blood pressure can lead to edema or drop of blood pressure could lead to the dehydration but we had said that a drop in blood pressure is about hypotension or shock shock means low blood pressure this is called circulatory shock it is a drop in blood pressure because you don't have enough of this hormone now you'd say is that will you die from this would be very critical but you'll be dead before you reach this point you'll be dead because of the other thing that it causes hypo of Austrian is it means you look if you don't have enough aldosterone you don't excrete the excess potassium so let's imagine you've got this condition and you ate those three bananas you ate the three bananas you raise the potassium levels in your blood you now have hyperkalemia but without this hormone you don't get rid of that excess potassium because now you retain potassium rather than excreting it though this hormone normally causes your kidneys can get a little bit excess potassium but you don't have this hormone so now you develop hyperkalemia and as you answered on the cata test hyperkalemia leads to depolarization of all the cells in the body and as all the cells start depolarizing they start firing off action potentials that occurs in your nervous system increased electrical activity in your nervous system and brain increased electrical activity your skeletal muscles but what you die from is increased electrical activity of your heart your heart rate gets faster and faster mastered fashion goes into fibrillation and you talk so that that occurs that's what usually kills the person is the heart going into fibrillation from hyperkalemia that it's really the heart function that is the most critical one you is affected by elevations or decreases in potassium levels it affects all electrical activity and everything with that heart when the heart rate starts getting too slow or too fast because of either hypokalemia or hyperkalemia then you're in big trouble alright so that's it was on page 42 or we really talked about that so now we've spoken of this let's turn all the way to page the very last page of the cardiovascular system page 272 to 72 what is a normal blood pressure we're going to be learning a lot about blood pressure as we move on in to cardiovascular physiology the normal blood pressure is usually said to be about 120 over 75 120 over 80 now of course when you hear these numbers for blood pressure that's your blood pressure in your brachial artery of your arm because that's where they put that cuff that's blood pressure is different in different blood vessels of your body that's just where it is what it is in your brachial artery so we'll be learning that you've got all kinds of different blood pressures we previously learned that the blood pressure your capillaries is around we've learned 26 millimeters of mercury and your Catalans the units here are millimeters of mercury or Torr now why are there two numbers and why not just one we'll get to that we're going to explain why there's a high number and a low number because your blood pressure goes up and down and up and down now before the break we mentioned that high blood pressure is called hypertension the definition of having high blood pressure is a blood pressure greater than 140 over 90 nowadays they also talked about being borderline I have a borderline high blood pressure 135 over 85 but certainly doctors normally aren't necessarily going to put you on any medication until you go about 140 over 90 now we mentioned before the break about one out of every five adults in this country have high blood pressure that's a lot 20 percent one out of everybody the etiology the word etiology means caused and we learned that there are two major causes of high blood pressure and again they further subdivide those earlier today we talked about two types of diabetes diabetes insipidus from deficiency of ADH and diabetes mellitus which is because of having too much sugar and we know that there's different types of diabetes mellitus right there's a juvenile onset and late onset so everything gets more complex the the main thing we learned is that essential hypertension which is what most people have technically it means we don't know what the cause is but there's a general consensus that it's probably due to atherosclerosis and that's why there's so much emphasis in reducing cholesterol levels and fat levels which lead to that buildup of on the walls of the arteries there's the second type of high blood pressure we've learned called renal hypertension due to excessive amounts of that renin-angiotensin-aldosterone mechanism I have done this is where they have dosterone causes the kidneys to retain excessively excessive amounts of salted water raising the blood volume attributing edema and raising blood pressure now most people have either one or the other could you have both types at the same time of course you can have any combination you can imagine now there are many medications used to control blood pressure but among the two most common categories of drugs used to control high blood pressure are these two right here sympathy lytx or also known as adrenergic blockers or beta blockers if we ever learn about those because we know that stress raises blood pressure and therefore if we could reduce the sympathetic response of the on the body that they can be used to reduce blood pressure this second major category of drugs commonly used to control blood pressure are drugs that reduce that inhibit that block the renin-angiotensin-aldosterone reflex now clearly this category would be very appropriate for renal hypertension wouldn't it because that's the problem is too much renin-angiotensin-aldosterone going on so that certainly makes sense to reduce that they do have more reviews these drugs even for essential hypertension but in general they tend to use the beta blockers more for essential hypertension but again they there's a combination another thing you will learn will you get in your clinical programs since we say there's different types of high blood pressure we tend to see different types of high blood pressure at different people because there's genetic factors so we know that people of say African ancestry are more inclined to have renal hypertension and Caucasians more likely to have essential hypertension again people can have both but you'll learn that there are because there's genetic factors there are there for ethnic factors at this it is just genetics now I want to give you a couple of examples of drugs that block the renin-angiotensin-aldosterone reflex so let's go back to 134 G okay all of 134 G that's this diagram now I've listed a number of drugs there's only one that I'm going to ask you to know is 130 fortunate if somebody does have a hyperaldosteronism which leads to renal hypertension it certainly makes sense to try to reduce the South Ostrow the very first drugs I'm not going to ask you to know this but they're among the earliest drugs they use to try to reduce aldosterone of action and stimulating the kidneys to retain salt and water which leads to renal hypertension were aldosterone blockers drugs that block the aldosterone receptor sites on the kidney if you've ever heard of the drug spironolactone which goes under brand-name Elva docto you heard of that this is still widely used it's a very important drug it's known as a potassium sparing diuretic they are still very important I'm not asking you to know it but you promise you you will learn it ok it's a very important drug but that blocked the aldosterone receptor sites on the kidney which now give this this is not all or nothing all drugs work it's dependent on dose as you increase the dose you get more and more blockage so obviously they just want to titrate it and reduce the amount of dosterone stimulating the kidneys so that the kidneys aren't retain retaining as much salt and water as it had and that should reduce the renal hypertension then after they develop those a number of years later they said well you know since it's really angiotensin ii that's causing the adrenal cortex to release the aldosterone let's develop drugs that block the angiotensin ii receptor sites on the adrenal cortex so then they developed angiotensin 2 blockers an example of this and I'm not asking you to know it as a drug called Kosar they've ever heard of Kosar it's another one you'll hear about more recently after they discovered that what's actually creating angiotensin 2 is this enzyme in the lungs that converts angiotensin 1 and angiotensin 2 they develop drugs that inhibit this enzyme these are called angiotensin converting enzyme inhibitors or AC II inhibitors very very important these are really very popular in common right now and all of the and these I do want you to do I want you to know what an AC inhibitor is these are all these drugs that are AC inhibitors go have brand names that end in IL zest drill a q prim plena Vil that so they all tend to sound like that there are exceptions so I want to show you an example of this so you have a handout there that we gave you so this is from a drug book we've already mentioned that drug books don't have pictures this is a drug called Quin Aprill now I'm not testing you on knowing the name of this drug I want you to know how this category of drug works so Quinn Aprill goes under the brand name a cube root again you don't have to know these drug names you'll be asked to do that when you have part mycology having memorized names but here's the point that I do want you to know I think I believe that there's an arrow here and so what is the pharmacologic category does everybody see that this drug is called an angiotensin converting enzyme inhibitor and what does its uses in the management of hypertension high blood pressure and congestive heart failure now I'm not going to get into all this stuff look on the flip side of this all right so under mechanism of action or I have an arrow so how does the how does this drug work it competitively inhibits the angiotensin converting enzyme or AC e preventing the conversion of angiotensin 1 to ng to now talks about some other things that angiotensin 2 does because angiotensin 2 which I'm not asking you to know also constricts blood vessels but you'll notice it also says just a little bit below that that there's a reduction in aldosterone secretion because if you prevent the conversion of angiotensin 1 and angiotensin 2 there's less stimulation of the adrenal cortex to secrete aldosterone this is a very widely used class of drugs you see this right so so I do want you to know in a CEU hibbett risk why they will they wanted what they want to do is they actually the trend is to develop drugs that are blocking earlier and earlier in this sequence because therefore each time you forms the next chemical even though this diagram shows that the chemical has only one effect it's actually having a multiplicity impacts and they want to back this up further and further you know and they're really eventually going to have something that stops the release of right that that's what they're working on so the idea is just to keep backing it up further earlier and earlier in this mechanism okay the other handout that I gave you is this now there's nothing I'm asking you to know on this but just before you throw it away I I mentioned earlier today that whatever hormones I cover they're discovering that there's just hormones being produced by every part of our body this this is not yet in any of your textbooks at least at this level this is basically new information that is only developed in the last few years that's only in journals but this comes at a Columbia University of Medical Center where they have identified the skeleton now as a meaning the bones are an endocrine organ they have made that it appears that it secretes a hormone that helps control the sugar metabolism and your weight especially in type 2 diabetes where there's a problem so the you name they name this hormone osteocalcin now it not because it affects calcium levels but it's produced by bone cells is osteo so that's the name they've given it and you can read the article but here's the also they mentioned there is another hormone you may or may not have heard of called leptin leptin is a newly discovered hormone secreted by fat cells and that also affects metabolism so we're starting to see every type of cell in the body of secreting hormones so as I said earlier this whole kind of concept of an endocrine gland is breaking down now the anatomy classes will still continue to teach it but in Physiology it's becoming more and more difficult to talk about a classical endocrine plant what we have learnt already that adrenaline or epinephrine produced by the adrenal medulla is a neurotransmitter produced really by a ganglion of sympathetic autonomic motor neurons oxytocin is a neurotransmitter right it's not see if it's secreted by an endocrine gland screwed by hypothalamic neurons so you know everything is breaking down and here's the main point of this people with type 2 diabetes have been shown to have low levels of osteocalcin so if it turns out that this new smoothly discovered hormone secreted by bone cells is actually maybe the cause of type 2 diabetes so they're going to be developing a synthetic osteocalcin to give to people because they've got abnormally low levels all right getting the last thing on the flip side of this in terms of diabetes now and many of you are aware of what i'm about to say you know diabetics classically who needed to insulate have to inject it two or three times a day this is a big problem nobody likes having to use syringes and needles and they have to guess the amount of it so what they need sometimes they guess wrong and they've given themselves too much insulin and their blood sugar levels too low so this is a huge problem for they have to because they have to guess what their insulin levels are needed so the new approach now and I think again maybe you know this is to where an insulin pump the insulin pumps they may see anybody with an insulin pump this is like a device it's connected by a catheter to the bloodstream they wear it all the time and it the blood flows through this device it senses what the sugar level is in the bloodstream and depending upon what the sugar level is it releases varying amounts of insulin they don't have to eject themselves with a syringe and it's much more accurate and it only releases the enough insulin to keep their blood sugar levels normal that's the best thing other than the other than having the real pancreas do it so everybody's moving to these insulin pumps you don't even take it off it can't it's connected into the blood stream it's the catheter goes into your body I mentioned this in the afternoon class they say well that's like so weird you've got this thing permanently connected to your body if you know of anybody who has a pacemaker for their heart you know what a pacemaker is it's a battery-powered electrical stimulator surgically positioned under the skin and that's connected by a wire to the heart and they wear it it's under there in their chest and it's all the time stimulating their heart to keep beating

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Keywords: RENIN, ANGIOTENSIN, ALDOSTERONE, ACE Inhibitor, Angiotensin, JG cells, Endocrinology, Hyperaldosteronism, Hypoaldosteronism, ADH, hyperkalemia, Angiotensin Converting Enzyme, spironolactone, angiotensinogen, Renal Hypertension, hypervolemia, circulatory shock, Blood Pressure, Blood Volume, professor fink, www.professorfink.com, anatomy, physiology, anatomy & physiology, anatomy and physiology, hormone, hypokalemia, juxtaglomerular, Kidney, Renal

Id: IUIokwmJJRM

Length: 46min 53sec (2813 seconds)

Published: Mon May 07 2012