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Bye. OK. Everyone should be able to see a screen now. So OK. So it's fine now. Yeah. OK. Uh Hi guys. Sorry for the late start, basically. Um But today we're gonna go through renal regulation of water ions and electrolytes and then we're also gonna go through a antihypertensive. Um Basically. Um OK. So renal regulation of water, basically, this is just how water is reabsorbed along the Nephron. So, in the Nephron, you've got your proximal tubule, your descending ascending limbs, your distal convoluted tubule and your collecting duct. Um So proximal convoluted tubule, descending limb. These are passive um as well as your collecting duct and your ascending and distal convoluted tubule are impermeable. Um And it's really important to not that water reabsorption is basically a passive process because um the body doesn't want to spend too much energy, absorbing water or conserving water, that kind of thing. And the best way to do this then is to create a concentration gradient. So the medullary interstation will need to be hyperosmotic for your water reabsorption to occur from the loop penny and from the collecting duct and that kind of thing. So these are probably the most complicated parts of the lecture. So, cancer current multiplication, um rear recycling that kind of thing and it can be a little bit hard to wrap your head around. But basically the kidney needs to reabsorb water efficiently to concentrate your urine. And that happens by establishing a gradient in the medullary interstit, which is basically just the space around the loop of Henle. So the liver penny has two parts that work together. You've got your descending limb, which is permeable to water, but not to salt. And you've got your ascending limb, which is impermeable to water. But part of it will actively pump out salt that the descending limb will actively pump out salt. Um So it's a step by step process. And the easiest way to think about it is by thinking of the thick ascending limb or the ascending limb first before the descending limb. So your filtrate will enter the loop of Henley at let's say 300 milli osmoles um or like roughly the same blood, the same as your blood plasma basically. And then your ascending limb will actively pump out your salt. So you've got passive um so um diffusion and then you've got your active salt um pumping being pumped out of the thick ascending limb because your water can't follow the filtrate inside the ascending limb will become more dilute. So your osmolarity will decrease to around 200 with the osmoles instead. And because you're pumping out loads of these salts. The inter the interstitial space will become a lot more saltier so that your osmolarity will increase basically. So around 400 mill osmoles. So you've got roughly, you've got like more dilute inside and hyperosmolar outside. Then you should think about the descending limb. So our descending limb is permeable to water and because our interstitium is hyperosmolar, now, our water is going to move out into the interstitial by osmosis. And that's gonna make your filtrate inside the descending limb more concentrated. So let's say our filtrates at around 400. Now, and now you've got more filtrate moving into the descending limb. So this is a constant continuous process. So the fluid is constantly moving through the Nephron. So our new filtrate is entering at the descending limb, pushing down the already processed filtrate further along. And the cycle basically repeats and repeats and repeats. So more salt is pumped out from the ascending limb, more water moves out of the descending limb and over multiple cycles, you're basically just creating a really steep osmolarity gradient. So the outer Ella is gonna be less salty, roughly 300 m osmoles where and the outer mela by the way is like the top of the Nephron. Whereas the inner medulla like deep into the loop of Henley, that's gonna be very salty around 1200. So the really key thing to understand is just that with every new cycle, your gradient basically expands deeper into the medulla. So at first, the gradient difference might just be 300 to 400. But then with each cycle, because salt is being pumped out at multiple levels. And because your water is following and because the water is basically pushing down um the filtrate further into the loop of Henry, you're going to increase the maximum osmolarity at the inner medulla. So um the the most hyp the hyperosmolar part is going to be basically the bottom of the loop of he. And this is basically important because you want to create your osmotic gradient. And it's essential for the collecting duct to basically reabsorb water when needed under the influence of ADH. It also allows you to concentrate your urine and prevent water loss. And if you're thinking about why is it called cancer current multiplication, we say cancer current because the filtrate will flow in opposite directions. Uh So the descending limits going down and the ascending limits going up and multiplication just because the process is amplifying the concentration gradient with each cycle basically. So then Nephron mechanics. So we've got uh Urea recycling. So the loop, he alone can't create a massive massive gradient just by moving sodium and water. We also need a few other things. So, urea is a key player in boosting our osmolarity of the medullary interstation. And that basically just ensures the kidney can reabsorb more water from the collecting duct. So initially, urea is trapped in the collecting duct. Um because in the cortex and the outer medulla, the collecting duct is impermeable to urea. So it gets concentrated as water is reabsorbed. But then in the inner medulla, the collecting duct becomes permeable to R urea, especially under the influence of a DH. And urea will basically then just passively diffuse out of the collecting duct and into the medullary interstation. Um Once urea is in the incision, it will help to increase the osmolarity of the in a medulla. And that is crucial for water reabsorption. So, once the uh urea has left our collecting duct, it basically has two fs. So some urea can enter the vasa reca which is just the capillary surrounding the Nephron, basically where it gets carried away. Um And then some urea can get reabsorbed back into the descending limb of the loop of he, which is basically a recycling part. So the recycled urea will follow the filtrate through the Nephron again and it'll reenter the loop of he travel through the tube, you'll reach the collecting duct, some will be reabsorbed and that kind of thing. Um And that repeats and repeats and repeats and you're basically just maintaining your high osmolarity of the inner Mandela. Um So you can kind of think of urea as a booster for the kidneys concentration ability. So, instead of just relying on sodium and water movement, uh the kidney basically recirculates urea to maintain your hyperosmolar medullary interstit and that will allow for your maximum water reabsorption when needed. Um And if you also want to think about ADH or vasopressin, that helps to boost uh uta one and uta three transporters, which you can see on the diagram up there. And that basically increases the collecting ducts, permeability for urea and aids urea reabsorption. So, ADH and this is a hormone you should have heard of before, which promotes water absorption by the kidneys nephrons. And how it works is it basically reaches the collecting duct via the blood. It binds to V two receptors on the basolateral membrane of the collecting duct that will trigger a G protein kinase signal cascade which will activate protein kinase A um and that will increase your secretion of aquaporin two channels in a vesical form. And they're then inserted into your apical cell membrane. Water is then reabsorbed through the aquaporin two and then through aquaporin three and four in the basolateral cell membrane. And then it enters the blood basically. Um but overall antidiuretic hormone up or down regulates aurin two on the apical membrane and aquaporin three on the basolateral membrane. And those numbers as required. Basically. Um A DH also then promotes sodium reabsorption at different points of the Nephron. So uh um loop of he distal convoluted tubule and collecting duct which will drive our passive water reabsorption. So it basically up regulates the number of transporters and those are the exact transporters you're looking at, so your sodium potassium chloride symporter or your triple pump, uh triple symporter, your N ACL S importers and your sodium channels. Um So, so you need to be thinking about stimulation and inhibitory factors of ADH release. And basically, if you're thinking about stimulation, you're thinking about signs of hypovolemia or low blood blood volume. So that can be increased plasma osmolarity, decreased BP and.