1. Regulation of Body Fluid: Regulation of Water Flashcards
What must the thick ascending limb maintain between the tubular fluid and the interstitium at any point along its length?
200mOsmol/kg H20
What is the maximum osmolality at the tip of the loop of henle?
1200-1400mOsmol/kg H2O
What is the state of the fluid when it leaves the loop of henle and enters the distal convoluted tubule?
100mOsmol/kg H2O, HYPOTONIC solution meaning the cells will swell in this solution
The first step in the coutnercurrent multiplier is when the tubular fluid enteres the descending limb from the PCT and is isotonic (PCT is always 300mosm). Before the gradient is established, the medullary interstitial fluid concenctration is?
300mosm everywhere
The second step of the countercurrent: thick ascending NaKClCl transporter pumps NaCl into the meduallary interstitium until there is a 200 mOsm difference, this causes?
The fluid in the medullary interestitium will then become hypertonic, more concentrated, leading to water from the thin descending limb to permeating into the interstitium
In the 3rd step, water passivle moves until it is at equilibrium with the interestitium. The fluid in the ascending loop of H becomes more concentrated due to?
more water going into the interstitium to equilibriate, ascending LoH is at 200 and interstitium and descending are at 400mosm
The same steps are repeated over and over again with the descending limb progessively getting more hypertonic until it reaches 1200-1400mosm. What about the fluid before leaving the ascending loop?
the fluid is hypotonic at about 100mosm before entering the DCT, about 1/3 of the original osmolaltity
The vasa recta supplies blood to the medulla, and is HIGHLY permeable to solute and water. The ability for it to maintain the gradient is flow dependent, if there is an increase in blood flow, it dissipates the medulary gradient causing medullary washout. What happens if there is a increase in blood flow?
decreases salt and solute transport by nephron segments in the medulla reducing the ability to concerntrate the urine
Urea is recycled when concentrated urine needs to be formed or when there are high levels of ADH. With high levels of ADH, reabsorption of water from the distal tubule and cortical collecting tubule increases, increasing the tubular fluid of concentration of Urine. What does urea then do when ADH is present?
Via the UTA1 and UTA3 transporters in the inner medullary collecting duct, urea diffuses into the medullary interstitium which diffuses into the LoH through UTA2 , concentrating the urea
There are two things that create the medullary interstitial gradient. One: the combination of aquaporin channels and absence of tight junctions in the thin limb provides pathway for H2O to move w/o sodium following. Two:?
The anatomic arrangements of the LoH and collecting ducts which increases the osmolality as the loop dips deeper into the medulla
What is the location of the the two large neurons in the hypothalamus which synthesize ADH?
supraoptic and paraventricular nuclei of the hypothalamus
When the supraoptic and paraventricular nuclei are stimulated by increased osmolarity and other things, a nerve impulse passes down the nerve endings, doing what?
changing their membrane permability and increasing calcium entry. (ADH is stored in the secretory vesicles of the nerve endings, occurs within minutes)
Osmoreceptors are sensitive to small changes (1-2%) which releases ADH and stimuates thirst. Which usually occurs first?
ADH released and then thirst activated
The late distal tubule and collecting ducts have two cell types including the principle cells and the intercalated cells. What do the principle cells reabsorb and secrete?
Reabsorb Na+, Cl-, H2O and secretes K+
Principle cells reabsorbs Na via NaKATPase, H2O via ADH, which increases permeability via AQP2 in the apical membrane in the late DCT and CD. How is K+ secreted here?
K+ is uptaken from the blood via NaKATPase, and then passed down its gradient throuhg the Kchannel into the lumen urine
***Aldosterone increases this process of K+ excretion and Na+ reabsorption
Intercalated cells reabsorb K+ and secrete H+ how?
Via aldosterone, which stimulates the H+ATPase in the intercalated cells (along with what it does in the priciple cells)
Steroid aldosterone causes an increase in the number of ENaC (epithelial Na Channels) located on the apical side transporting more Na into the cell to be reabsorbed. If more Na is reabsorbed via the NaK ATPase, what does this mean for K+?
K+ will increase in the lumen and more will be excreted d/t increase in aldosterone.
There are four main ways aldosterone is activated.
1. Rise in plamas K+ directly stimulates adrenal cortex to increase its output of aldosterone. What are the other 3?
- A decline in K+ plasma reduces aldosterone secretion
- decrease in plasma Na stimulates aldosterone secretion via RAAS system
- Increased aldost promotes simulatneous Na reabs. and K+ secretion*****
AQP2 is in the apical membrane of the medullary CD and DCT. When present due to ADH/vaspressin/AVP, they do what?
An increase in AQP2 would lead to an increase in reabsorption of H2O, creating a more concentrated urine. Vice versa if there was a decrease in AQP2 d/t decreased or absent ADH
What are the steps of our body responding to increased osmolality?
When concentration is increased, signals to the hypothalamic osmoreceptors, secreted ADH which travels to kidneys where stimulates AQP2 and thirst, which increases reabsorption of H2O, increase urine concentration and excretes extra solute
What are the steps for our body to respond to decreaseed osmolarity?
Osmoreceptors in the supraoptic and paraventricular nuclei of the hypothalamus trigger cessation of release of ADH so collecting tubules remain impermeable to water, increasing dilution of urine and excreting more H2O to get concentration back to normal
An adequately hydrated person has a osmolarity of 275 to 295 while a dehydrate person would have a osmolarity of >300. What are the simple rules for ADH?
Overhydrated = ADH inhibited Dehydrated= ADH released
Diabetes insipidus has 2 types. The first type is failure to produce ADH from posterior pituitary due to head trauma, infections, or congenital- central neurogenic diabetes insipidus. What is the second type?
Inability of the kidneys to respond to ADH: Nephrogenic diabetes insipidus
In central diabetes, the distal tubular segments cannot reabsorb H2O, resulting in a large volume of dilute urine (15L/day). What is the main treatment for this disease besides water restriction?
Demospressin (analog of ADH) which acts on V2 receptors to increase water permeability in late distal tubule and CD.
restores urine back to normal, stronger concentration
