BISC 307L 2nd Edition Lecture 39 Current Lecture On left are the responses of the body to a decrease in blood volume and blood pressure The most common causes of this are dehydration and hemorrhage Decreased blood volume and blood pressure will boost cardiac output and the hypothalamus will stimulate a desire to find and drink water The kidneys play a very important role as well because they can minimize water loss through the urine The ultimate solution to the problem is drinking and getting more water But the kidney can at least prevent further loss of water It is not obvious from this diagram but there are two different types of pressure receptors or baroreceptors in the body They are in the carotid body and aortic body They are referred to as the high pressure baroreceptors But in addition to that there are a set of low pressure baroreceptors They are stretch sensitive nerves in the atria the pulmonary vasculature and the big veins So these are highly compliant parts of the vascular system And because these are low pressure highly compliant parts they tend to expand So these low pressure baroreceptors are often called volume receptors Whereas the high pressure baroreceptors are called pressure receptors The reflexes that get activated when pressure is too high or low are one set they overlap but they are distinctive in other ways from the reflexes that kick in when blood volume is too high or too low and these two sets of receptors is what sense those differences Water Balance in the Body In order to not gain or lose water the body has to be in water balance You would gain 2 5 liters of water a day Notes 1 Not including intravenous infusion 2 Mostly from aerobic respiration fuel molecules O2 CO2 H2O 3 Not including diarrhea vomiting So water input has to equal water output and things need to be in balance No matter how much water one drinks we ve already seen that a variable amount of plasma gets filtered into the kidneys So way over 99 of that water has to be reclaimed Most of that reclamation happens in the proximal tubule A little more happens in the loop of henle and part of the distal tubule which leaves the rest of the distal tubule and the collecting duct as the places that do the final adjustment of how much water is excreted from the body Osmolarity Within Kidney This is a picture of the osmolarity within the kidney Can see the juxtamedullary capillary with the long loop of henle and as you know the kidney has this osmotic gradient in it where the cortex and outer medulla have an osmolarity of about 300 mOs M which is about the same as blood But as you go deeper away from the outer medulla it gets more osmotically concentrated It gets up to 1200 at the deepest part due mainly to high concentrations of salt and urea The cells in here have to have special adaptations to keep from being denatured by this special salt and special urea In the little yellow boxes are shown the osmolarity of the tubular fluid at different strategic points along the length of the tubule The filtrate in the bowman s capsule of 300 has the same osmolarity of blood And as the fluid is pushed by the net filtration pressure along the proximal tubule it ends up along the proximal tubule still being 300 We know that water is reabsorbed but we also know that it is done so by reabsorbing the solute and allowing the water to follow so the osmolarity overall stays the same So the fluid is at reduced volume It enters the loops of henle at 300 mOsM Keep in mind that epithelial cells in the descending loop of henle are permeable to water but not to salt So there are aquaporin channels and leaky junctions The ascending limb of the loop of henle is permeable to salt but not water So given that there is an osmotic gradient what happens is that tubular fluid at 300 comes down and water leaves by osmosis And salt cannot follow So the fluid in there gets increasingly salty So by the bottom of the loop the tubular fluid will be as osmotically concentrated as the surrounding interstitial fluid The water that leaves gets reabsorbed into the vasa recta it doesn t just stay around and dilute the interstitial fluid So the fluid takes the hairpin bend and starts getting pushed upward The walls of the tubule of the ascending limb are permeable but not to water In the thin part of the ascending loop there are no active transporters it is just permeable to salt And as this salty briny fluid comes up the tubule it is increasingly moving int o an environment where the interstitial fluid is less salty So there is a gradient for salt to go out And it does go out And as it goes out the tubular fluid becomes less salty It comes into equilibrium with the interstitium around it When you get to the thick ascending limb it is thick there because these are big beefy cells that are packed with mitochondria And the reason they have mitochondria is because they carry out a lot of active sodium transport The passive movement of salt out in the thin ascending limb gets replaced with active transport of salt in the thick part This is necessary because the concentration gradient for salt to go out gets smaller and smaller as you go up To ensure that more salt is being absorbed active transport takes over and salt is actively extruded from the tubular fluid This salt that comes out contributes to the salty inner medulla But this is happening all day long the excess salt gets reabsorbed back into the vasa recta So much salt is pumped out of the thick ascending limb by the time you get to the top the osmolarity of the fluid is lower than that of body fluids Reabsorption of Na K and Cl in the Ascending Limb The important organ here is the Na K pump in the basolateral membrane All these ions going to the right being transported out of here are being moved by the Na K pump This transporter is unique to this part of the nephron And it is important to realize that because there are drugs that can be used to get rid of water from the body or not that target this transporter So this transporter brings one Na one K and 2 Cl in The sodium ions that come in get pumped out The potassium ions go through potassium channels or potassium symports in the basolateral membrane And the chloride goes out of chloride channel or goes out with potassium through that symporter Notice the water cannot follow and gets left behind so tubular fluid can become hypoosmotic And this is the only part of the nephron that can create a hypoosmotic fluid and this is
View Full Document