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0:06
all right ninja nerds in this video we're going to take a nice brief overview of everything that we've covered throughout the series of videos in the renal playlist so you guys have already watched it about the proximal convoluted tubule you guys have watched the glomerular filtration process the loop of Henle the distal convoluted tubule and the collecting duct videos then what we're going to do is we're going to take a nice little brief overview over that just to make sure
0:26
that we got all of this stuff clear alright so let's go ahead and start that so if you guys remember what do we say what's happening well we said that this was the a fairy material right coming in to the actual glomerulus and the glue Maris was that set of capillaries that was the filtering structure right and what did we say here was happening we said there was a mixture of pressures right the pressures that was trying to push out was the glomerular hydrostatic pressure which is inside of the
0:48
capillaries exerted by what the blood pressure the systemic blood pressure then what else do we say we also said that there was an osmotic pressure of the AAB specifically the proteins with inside the actual blood then we're trying to pull water into the blood stream then we said that there was a capsular hydrostatic pressure that was actually going to be due to the filtrate trying to drain sometimes some of that filtrate can back up and exert a pressure trying to push certain filtrate
1:13
back into the actual maelys that was called the capsular hydrostatic pressure and then we say that there was a capsular osmotic pressure but it should be zero because there should be no proteins plasma proteins like albumin that should be filtered across this membrane because if you remember the capsular osmotic pressure was trying to pull fluid out into the glomerulus space alright so now that we know all of those again we remember what was the overall outcome of this we said that there
1:38
should be a net filtration pressure of approximately ten millimeters of mercury right we said that that's what it should be the net filtration pressure should be approximately about ten millimeters of mercury what else do we say remember that relationship we made with net filtration pressure we said the net filtration pressure was directly proportional to the glomerular filtration rate and we said that the glomerular filtration rate should approximately be about 125 milliliters
2:05
per minute we did that calculation in the glomerular filtration video so that is our GFR the glomerular filtration rate which is directly proportional to the net filtration pressure is how much fluid in volume per time is being filtered across this actual glomerular filtration membrane and we said a lot of different fluids are being pressed across this membrane right before we do that though what was this actual arterial here supplying the glomerulus do you guys remember this was the a
2:33
ferrant arteriole right and we said that this was one of the weird example of a body that in a capillary bed was actually fed bar inner cereal and then drained by an arteriole so this is an example of a efferent arteriole because this is actually draining the actual capillary but then what do we say this filtration process occurs across the membrane a lot of fluid and a lot of different different types of filtrate substances are actually going to be accumulated across this area and drained
3:05
into this next structure here what is this next structure here we said that this is the proximal convoluted tubules and this is one of the more important sites of the actual nephron what is a nephron you guys remember we said in Efron was the glomerular capillaries plus the Bowman's capsule right which is made up with a visceral layer which is the podocytes and the parietal layer which is made up of those simple squamous epithelial cells that made up the renal corpuscle
3:30
plus the proximal convoluted tubule the loop of Henle and the distal convoluted tubule that was a nephron and we have about 1.2 million in one kidney so if we have two of them generally unless you have renal agenesis unilateral generally you're going to have two kidneys and it's gonna be about 2.4 million right so that's pretty cool anyway we get the proximal convoluted tubules what did we say happens in this area a lot of reabsorption a lot let's start with that
3:54
first and then we'll talk about the secretion mechanisms so we said a lot of sodium was reabsorbed here we said a lot of water was reabsorbed here we said a lot of potassium was reabsorbed here a lot of chloride a lot of magnesium decent amount of calcium is reabsorbed here and what else did we say was very absorbed here bicarbonate so exactly about how much of these guys there was more will mention a couple of other ones right but sodium about 65% of the actual sodium
4:27
reabsorbed what do we say was really important about that we said that because 65 percent of the sodium is reabsorbed water-filled obliged to follow and we said that that we approximately about 65 percent we said bicarb generally depending upon the body's demands generally about 90% of the bicarb is reabsorbed about 85 to 90 percent magnesium it's kind of questionable certain literature will say different we're just going to say it's question about the amounts of magnesium
4:57
that are going to be reabsorbed potassium is around the range of about 60% okay around the range of about 60% and chloride ranges to about 50 to 60% also all right calcium about 60% of the calcium is reabsorbed here we said right 60% of the calcium is reabsorbed here a lot of different things reabsorbed here and again what is the definition of tubular reabsorption we said tubular reabsorption is defined as the process in which substances from the actual kidney tubules this filtrate is moving
5:30
where we said that these substances are moving from the actual kidney tubules where into the blood all right from the kidney tubules and into the blood so if this sodium is moving this area this water is moving to this area this bicarb is moving to this area and the magnesium and the potassium and they're going into the blood this is defined as tubular reabsorption we talked about many of the mechanisms how sodium is brought in how water how by car we're not going to do
5:58
that we don't need to write but one thing I do want to mention is what actually is brought in with sodium and what is also going to be another process talking about just a second remember glucose one of the organic nutrients and amino acids amino acids these substances did what remember they actually went with sodium the sodium glucose and sodium amino acid code transport mechanisms those were also important so glucose and amino acids were also reabsorbed in this process dependent
6:30
upon the actual presence of sodium we said what else do we say gets reabsorbed small amounts of your real gets reabsorbed let's use this actual green colors in urea so urea about 50% about 50% of the urea is actually going to get reabsorbed into the body right back into the bloodstream oh good question how much of the glucose in amino acids physiologically should be 100% if you have traces of glucose in the air and they call that glucose area right and usually glucose urea is
7:05
identifiable by someone who's actually having diabetes so that's not normal that glucose in the air because a hundred percent of that should be actually being reabsorbed and the reason why is we have these transporters here that are designed to be able to bring in the sodium and the glucose and they can bring that up until the blood levels usually the actual glucose levels in the bloodstream go above 180 milligrams per deal then the transporters are getting saturated and you reach was called a
7:30
transport maximum and then it starts getting lost in the urine okay so we talked about that what other things were being reabsorbed here not just urea and all these different electrolytes we also said that small proteins were being absorbed here too so small molecular weight proteins small proteins like insulin albumin we said even a little bit of the hemoglobin these molecules can actually get reabsorbed so small proteins can actually get reabsorbed into the bloodstream and we said it was
7:57
by an endo cytosis mechanism what else did we say we also said that lipids remember lipids they're really weird lipids actually get reabsorbed in this process too because what it's passed a diffusion they can diffuse right to the fossil of a bilayer so the lipids can also get reabsorbed into the bloodstream okay so we talked about lipids small proteins all of these different electrolytes and the organic nutrients what else and then leave in this metabolic waste urea what lots of things
8:25
that are being secreted how we define tubular secretion it's the process of moving things from the blood into the actual filtrate how does that happen well you know that we can actually excrete certain drugs in this area so we can actually take certain drugs I'm not going to go over the many drugs that you can actually excrete in this process but one thing I do want you guys to know is that in order for us to excrete drugs in order for us to excrete protons in order for us to excrete other
8:52
different types of metabolic waste products so other different types of metabolic waste products for example limonium and even small trace amounts of creatine are creatinine these substances here in order for them to get pumped over here it depends upon the presence of ATP we need ATP in order for us to be able to pump these substances from the blood and into the actual filtrate so all of these processes here require the presence of ATP ok now that's one thing
9:27
and not only can you actually push these protons out right depending upon what the situation might be if you're in a situation when you're in metabolic acidosis you'll pump the protons out you can also get rid of bicarb so there is certain situations in which you can actually lose by car but we'll talk about that when you get over to the intercalated B cells okay so for the most part this covers in general what we talked about in the proximal convoluted tubule video then as we get down to the
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loop of Henle what did we say actually before we do that what was the milliosmoles we got to make sure we bring up that milliosmoles of right the osmolality what do we say was the general flow as we move our way down okay we said as we move our way down goes from about what it goes from 300 milliosmoles and it works its way down work from that point let's see how that goes okay so you guys remember it starts up here at 300 milliosmoles and then it works downwards to about 500 millivolts
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then we get down to about maybe 700 millivolts then we get down to about 900 million moles and as we get really really deep down into the renal medulla you can hit 1200 milliosmoles now really really briefly let me show you what i'm talking about here in a side diagram let's come over here for a second just a real quick side diagram I draw a kidney here so we're clear let's say I take one piece here I take one lobe here okay and here's the calyx which is going to collect the actual
10:52
you're in at ripping off this is a renal pyramid the renal pyramid is two parts this part here is the cortex it's more of like the lighter granulated tissue and then the other part was the renal medulla and that was that nice little striated part right now was dude a lot of the kidney tubules now what we're trying to say here with this renal you know medullary gradient is that as you move your way from the cortex which is where the proximal convoluted tubule and the
11:17
distal convoluted tubule and even the glomerular capillary we moved down 300 500 700 900 12 under that's what we're saying so the actual osmolality or the medullary grading and increasing as you go down that's what we're trying to say okay so now that we got that let's come back over here for a second okay so what do we say was the plasma osmolality of the actual blood the blood plasma we said it was approximately around 300 milliosmoles and then we said due to the
11:48
filtration process as it's moving across we said it should be equal so isotonic right so this actual should be 300 milliosmoles in the proximal convoluted tubules these should equalize so they should be isotonic with one another then we said after all the reabsorption and secretion mechanisms when it comes out here into this descending limb it should be what 300 milliosmoles let's do this in a different color make it bright so that you guys remember so with this color
12:15
here one more let's do with orange let's make this 300 milliosmoles so whenever it's leaving when it's leaving the proximal convoluted tubule it's 300 milliosmoles okay sweet let's get back to this as we go up the ascending limb of the loop of Henle what do we say we had there remember we were pumping in from the filtrate we were pumping out sodium we were pumping out potassium and we were pumping out the two chloride ions right through the sodium potassium to cloud co-transporter and this was
12:48
happening along the entire length of the ascending limb and it was doing a lot of this right how much of this sodium this potassium and this chloride is actually getting pumped out well a decent amount not as much as in the proximal convoluted tubule but it's still a decent amount remember we said about 65% of the sodium here and it's about 25% of the sodium within the ascending limb for the potassium it honestly it ranges so generally they say it's approximately
13:21
about 30% and then for the chloride ions this is about 30% okay so again sodium 25 percent potassium 30 and chloride about 30 percent we're at the calcium and magnesium remember we were actually having what was happening remember some of those potassium ions with my green mark raise some of the potassium and some of the potassium lines were leaking back in because there's a different gradients right and then when the potassium was leaking back into this actual tube you'll lumen it was
13:53
generating a nice positively charged membrane depolarization right and what did that do it caused some of those calcium lines that was in this area to leak out remember there was calcium and there was magnesium and these ions started leaking out by that passive para cellular transport right out into the actual medullary space and they were also contributing to the medullary interstitial gradient making it saltier as you go down so what do we say we said if we had a lot of sodium a lot of
14:26
potassium a lot of chloride a lot of magnesium and a lot of calcium that was making the medulla really salty and then what do we say we said here that water's coming down he's like a lot of saltiness over there I gotta go so what happens a lot of the water starts leaking out through the aquaporin ones into the medullary interstitial space to where there's actual all these solutes particularly sodium and chloride right now when that happens what a lot of this
14:59
water is leaking out due to the sodium in the potassium and chloride and calcium and magnesium getting pumped out as it's going up what do we call that we called that D counter-current multiplier
15:19
mechanism right okay sweet deal so that was where a lot of the water is getting reabsorbed so a lot of the water is getting reabsorbed right here too so we said sixty-five percent there it's approximately about 25 percent here okay because right with 65 plus 25 55 plus 25 is zero Terry that one right there yeah so we're good yeah sorry so again about 25 percent of the water is reabsorbed right here reason why I did that because there should only be about 10 percent
15:50
left whenever we get up to the actual specifically the distal convoluted tubule okay okay 25 percent of the water we got all that part there now as we take this guy up okay as we take this guy up we're going to bring this actually should just not be 25 percent this should actually be 15 percent I'm sorry let me fix that this should be 20 percent water left over okay so as we bring this actual filtrate up what do we say okay we're going to look at the actual tonicity for this in order for us
16:24
to understand this we've lost a lot of water as we lost a lot of water out of the descending limb what are we losing then remember that the concept of tonicity we said there was hypertonic and then we said that there was isotonic and then we said that there was hypotonic hyper means that there's more solute less water isotonic means that there's a just an equal amount of water and solutes hypotonic means that there's actually a lot of water and left solute when we
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lost a lot of water if we lost a lot of ones that means that this is actually going to be hypertonic as compared to the plasma osmolality so right here should be hypertonic okay Queen so hyper sonic right there as we make the turn and we go up then when we do we're pumping out a lot of salt potassium chloride calcium magnesium and there's still about 20% of water left over if that's the case then as all this process is occurring throughout the entire length of the ascending limb by the time
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we go into the distal convoluted tubules what should it be it should be about 100 to 200 milliosmoles so this is very hypotonic right a lot of water very little salty it's not very salty and this is why that's why may that little mistake sorry 20 percent of it should actually be water and then a little bit of about 10 percent of it should actually be sodium okay all right cool so hypertonic as you get done with this one there should be hypotonic then as we went into the
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distal convoluted tubules so there was two parts the early distal tubules and the late distal tubules so you guys remember we kind of separated those kind of like right here right and what did we say happened we said with alien early distal two of you oh we had those sodium and chloride symporters right we were bringing the sodium in we were also bringing the chloride in and we were doing it through these actual nice protein channels but the only way that we could really do this was on the
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basolateral membrane what do we have we had those sodium potassium pumps which were comping the sodium right against its concentration gradient and the potassium against its concentration gradient approximately 3 sodium for every 2 potassium and what do we say this process required they required a lot of energy so required ATP but it helped to be able to do what it helped to be able to bring the sodium and the chloride in and then what could happen with these guys we said that the sodium
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could actually be brought out into the blood and the court could be brought onto the blood right and this is the process of reabsorption ok what else do we say could happen here we also said that at the other early part of the distal to build their specialized specificity depending upon hormones right remember there was that hormone that we talked about produced by a gland let's actually show them up here remember we had here the thyroid gland and then on the back of the thyroid
19:24
gland you had these tiny little glands here they were called the parathyroid gland and they were producing a special hormone and that special hormone was called the parathyroid hormone and what was the parathyroid hormone responding to it was responding to low blood calcium levels hypocalcemia so whenever there is hypo kalsi Nia this can be a stimulus to the parathyroid gland and cause the parathyroid hormone to produce to be produced and again what does hypocalcemia low blood calcium levels
19:56
when the parathyroid hormone comes over here what did he do remember he stimulated a g-protein coupled receptor and the overall result was the activated cyclic AMP II we're not going to go through the whole mechanism here but remember he activated cyclic AMP II which activated protein kinase a and what did that do that activated a specialized channel and this channel is not as a modulated channel right it's dependent upon parathyroid hormone so a protein kinase a does is he
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comes over here and phosphorylates that channel and what happens it allows for calcium ions that are still in the filtrate right because about 10 percent of the calcium is actually going to be coming about to this point here the calcium can get reabsorbed here but a defense upon that phosphorylation point and then what else did we say we also say that there were these transporters on the basolateral membrane that were pumping sodium in while you pump the calcium out into the blood to get the
20:54
calcium out here it's a blood stream to increase the blood calcium levels and it could be by this sodium calcium exchanger or it could also be due to another exchanger which is actually going to be let's put that one right here this could be due to protons protons would have to come in and then this calcium ions would have to come out and this would actually depend upon the direct utilization of ATP alright so this process right here would require ATP so we deal okay that was talking
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about the calcium reabsorption but again we said it was dependent upon parathyroid hormone you know what else is really cool about the parathyroid hormone that he's not only causing this calcium reabsorption he also deals with phosphates in the blood so you know in certain situations force phosphate actually reabsorbed come here for a second phosphate is actually reabsorbed right here let's you draw a phosphate and a let's do this one and actually just do this one black so here's the
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phosphate right so you have and usually it's in the form of hpo4 to negative right mono hydrogen fall State and what happens is this phosphate can actually naturally get reabsorbed into the bloodstream actually a good portion of about eighty-five percent of it is actually absorbed within the proximal convoluted tubules but if the parathyroid hormone is present if the parathyroid hormones present what it will actually do is is it'll actually cause phosphate excretion
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so what the parathyroid hormone will come over here and do is it will inhibit this process if it inhibits this process the phosphate is lost in the air and that cool yeah all right let's come back over here for a second another thing that I want to talk about here is right here this was this structure here remember we call this the basal recta we also had another special name for it he was also called the counter-current exchanger right he wasn't responsible for making the
22:54
medullary interstitial gradient this whole nice saltiness of the medulla he helped to maintain it right to prevent the rapid removal of the sodium chloride how did he do that remember we said some of that salt that sodium was pumped out here that potassium was pumped out here the two chloride ions were pumped out here what happens is as you move down well again what's that magic a inter social gradient like 300 500 700 900 1200 about right this is in milliosmoles as you go down and get saltier
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so what likes to happen then as you go down if you think about it if it's really really salty who's going to want to leave water water loves this salty stuff so as you're coming down water is actually going to start leaking out into this actual imaginary interstitial space okay and then salt is going to be really really rich in this area so it's going to actually move in so what will happen to this actual salt the sodium and the chloride ions will move in and as you
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think about that as you're going down is trying to equilibria with the actual medullary interstitial gradient so for example B 300 here 500 in here 700 in here 900 here and 1200 here but then when it makes the turn over here something really cool happens the exact opposite occurs now the water is going to want to come back in as the water starts coming back in a little bit of salt is actually thrown back out but here's what's really cool as the salt its thrown back out into the medulla to
24:32
prevent the rapid removal he keeps a little bit of that salt a little bit you wouldn't know how much okay what was it going in it should be 300 milliosmoles that's what we said the plasma osmolality is leaving it's just a little bit higher 325 million Wells so he helps to contribute to the rapid removal of the sodium and chloride from this medullary inter station to help to contribute and maintain the medullary interstitial gradient okay sweet deal that was there with the counter current
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exchanger then we got into the late distal tubules and that one we also said was actually very dependent upon a hormone what was that hormone that hormone was actually going to be aldosterone right and we said aldosterone was actually produced by what was produced by the adrenal cortex and we said there was a special part of the adrenal cortex here right it was called the zona glomerulosa and we said the zona glomerulosa is producing aldosterone and aldosterone is usually
25:34
stimulated whenever there's presence of angiotensin 2 or if the sodium levels in the blood are low remember we said the sodium levels in the blood are low in the potassium levels in the blood are high that could stimulate the release of aldosterone as well as angiotensin 2 is a stimulator of this ok and this is a stimulator okay da strands released what does he do we're not going to go over the whole mechanism we already did that we're going to say that he just stimulates
26:03
special genes right and those genes lead to the production of 3 different proteins one of the proteins was to get what get the sodium in then we said it developed another protein and this other protein that it made was designed to be able to pump 3 sodium out into potassium in so he's increasing the expression of the sodium potassium pumps right and these pumps required ATP because they're pumping things against their concentration gradient what else do we say it also made these channels
26:37
for the potassium to excrete the potassium out right so this potassium though is really high in the blood it's actually getting pumped out into the filtrate and the sodium that was really low in the bloodstream we're increasing it by bringing more sodium into the bloodstream okay so we're trying to bring in the sodium up and put the potassium down what a wise angiotensin to being stimulated because we have low blood pressure so there might not be enough of water in the bloodstream if we
27:04
bring more water in we can increase the blood volume and increase the blood pressure how does that happen remember there's another structure here let's draw this structure and about mammillary bodies hypothalamus anterior and posterior pituitary they're not testicles I promise we said that there's these specialized Osmo receptors that are stimulated right usually do the called organum vascular some of lamina terminalis a sub funicular organ they stimulate the Supra optic nucleus and
27:36
trigger the release of and - Doretta core Mon whenever the plasma osmolality is what whenever you have a high plasma osmolality what does that mean molality I'm allowing means whenever you have a high plasma osmolality that means that you have a lot of salt and very little water so what we're going to do we're going to release antidiuretic hormone answered erratic comas gonna work on the collecting duct the deeper parts of it and the cortical part here or like the
28:04
late distal tubules so look what happens inside a'right a corpsman can come over here and it can stimulate this cell to do what to make special aquaporins like aquaporin - so if we make these aquaporin two molecules what is that going to do that's going to open up these channels right they're going to make these channels that can pull water with it and if the water is flowing in what's going to happen the water can actually go into the bloodstream and if the water goes into the bloodstream what
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happens to the actual blood volume increases the blood volume which does what to the blood pressure increases the blood all right we deal there right so again now doctrine does what three things increases the sodium-potassium pumps makes the sodium channels to bring sodium in and makes these actual potassium channels to put potassium out and then the presence of antidiuretic hormone it can express aquaporin tubes which can bring the actual water and increase blood volume increase blood
29:00
pressure all right in the same way anted Rhetta Cuomo can act on the cells or the collecting duct look how he does it here remember which actually showed you that antidiuretic hormone we comes over here and binds on to v2 receptors and remember these v2 receptors of the basal press and receptors activated a g-protein activated adenylate cyclase which did what turned ATP into cyclic A&P and the cyclic AMP e activated protein kinase a you guys already know this what happens it increases the
29:35
expression I'm sorry not the expression it actually activates by phosphorylating these specialized proteins on these vesicles right remember it activates these specific proteins on the vesicles let's show you these proteins here in red I say here is these proteins on the synaptic vesicles and what does protein kinase a do protein kinase a comes over here and actually phosphorylates them and stimulates them to migrate to the membrane and what happens it plugs into
30:08
the membrane these little aquaporins and again this is aquaporin too and then what starts coming in water and if water starts flowing in what's going to happen the water will flow into the actual tubular cells and then there's these aquaporin 3 & 4 proteins we said on the basolateral membrane what will happen the water will go into the bloodstream as the water goes into the bloodstream what happens to the actual blood volume you're going to increase in blood volume
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which increases your blood pressure what else did we say well originally the plasma osmolality was high it was very hypertonic if we bring more water in we bring the asthma osmolality down back to a normal range of approximately 300 milliosmoles okay what else did we say remember we had the intercalated a thousand intercalated b-cells and they were functioning during metabolic acidosis and alkalosis remember what they were doing remember we had the a cell let's
31:14
say this is the intercalated a cell remember was actually taking the co2 combining with water to form carbonic acid right and then if you remember carbonic acid which age was h2 co3 which can disassociate into protons and bicarbonate and we said remember intercalated a cells us for acidosis so what does that mean we can pump proton out and who do we bring in a little bit of potassium right then what do we say if it's acidosis that means that the blood pH is really
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low what are going to do we're going to bring bicarb into the blood and what are we going to do to prevent excessive changes in the ions moving across this membrane we're going to bring chloride ions in if we bring a lot of bicarb out what you're going to do the pH it's going to bring the pH back up to normal ranges okay that was one of things we said then what else remember we had the intercalated B cell this was the be filling it was four basic conditions our
32:14
metabolic alkalosis right same concept what do we say here co2 combines with water when that happens what do you get you get carbonic acid this is driven by the carbonic anhydrase enzyme and again this is driven by the carbonic anhydrase enzyme this breaks down into bicarbonate and into protons what do we say is the difference here now we excrete aathi bicarb and we bring in the chloride ions right to prevent the excessive change there then what do we do we push the
32:47
protons out here why because we said that the blood is in a basic situation what does that mean that means that the pH is high if we bring a lot of these protons in what is it going to do it's going to bring the pH back okay and that's how our body deals with this metabolic acidosis and alkalosis situations what else did we say remember we also said that there can also be a little bit of certain substances that can be secreted out in this area too I draw one more cell here remember we said
33:16
we can actually have excretion of drugs we can actually excrete out ammonia remember we have ammonia and they can combine with one of these protons out here like for example this proton here let's say it combines with this proton that actually got pushed down what can we get out of this these two react we get ammonium and what else do we say that we could excrete - it could also excrete creatinine all right and there's even other substances that could also be
33:46
treated like uric acid and even a little bit of other nitrogenous waste products one more thing at the end part of the collecting duct what was that molecule that actually was left over a lot of water was lost so as a lot of water was lost out to extend this actual collecting duct down a little farther here and we get down as we get on to the bottom part there's just a little bit of all of this substance left over what color did we make him let's make him green this substance is called urea
34:19
remember your Rio was absorbed within the actual what the proximal convoluted tubule well some of the urea is actually reabsorbed here at the end of the collecting duct and what do we say that urea is doing we said some of that urea is actually being recycled remember it's actually moving over here and as it's moving over here to get recycled what happens some of that urea might accumulate here in the medullary interstitial space and urea is a solute it's more of a lipid soluble solute but
34:51
still nonetheless it can attract water because it can contribute to the medullary interstitial gradient what is that going to do that's going to allow for more water to flow out of what more water to flow out of the descending limb so it's going to contribute to making concentrated urine so again what does this process here called it's called urea recycling all right sweet deal and again a lot of that urea could actually get lost in the urine as well as well as
35:21
other substances that we'll talk about during the Victorian reflex when we talk about the composition in the urine okay so in a nutshell guys we covered a lot of this stuff here right one thing I didn't finish off with is this sodium in water I'm sorry twenty percent of the water right is remaining 20 percent of water because 65 percent of it was reabsorbed here and the PCT and about 15 percent of it was reabsorbed here in the loop of Henle specifically the descending the remaining water that's
35:51
left over is dependent upon the presence of antibiotic hormones so you the amount of water that you reabsorb is variable the sodium there's about 10 percent of the actual sodium remaining this sodium a small percentage about five to six percent of the sodium is actually to the sodium chloride symporter the remaining of four or five percent is dependent upon the actual odd Ostrom okay and then we said that calcium was dependent upon the parathyroid hormone iron is in this video we covered a lot
36:28
of information we covered basically everything that we covered throughout the series of videos I hope all of them made sense I really hope you guys enjoyed it if you did please hit the like button comment down the comment sections and subscribe
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