Osmoregulation and Excretion in Humans part 3 Flashcards
Overview
- While much of the absorption and secretion occurs passively based on concentration gradients, the amount of water that is reabsorbed or lost is tightly regulated. This control is exerted by hormones (directly by ADH and aldosterone, indirectly by renin and angiotensin)
- Most water is recovered in the PCT, loop of Henle, and DCT. But about 10% (about 18 L) reaches the collecting ducts. The collecting ducts, under the influence of ADH, can recover almost all of the water passing through them, in cases of dehydration, or almost none of the water, in cases of over-hydration
What do we know?
-Normally PCT reabsorbs all of the glucose and amino acids; about 65% of Na+ and water
- Descending limb of loop only permeable to water
- Ascending limb only permeable to solutes, actively and passively
- Hormones fine-tune reabsorption in DCT and collecting duct
- Most of the filtered water and solutes have bene reabsorbed before DCT
Osmoregulation: Reabsorption and secretion in the loop of henle
- The descending and ascending portions of the loop are highly specialized to enable recovery of much of the Na+ and water that were filtered by the glomerulus
- As the forming urine moves through the loop, the osmolarity will change from isosmotic to a very hypertonic solution to a very hypotonic solution
- Solutes and water recovered from these loops are returned to the circulation by way of the vasa recta
Solvents
-A solvent is a substance that can dissolve a solute
How are solutes measured
In weight
How are solvents measured
weight or volume
Osmolarity units
Osmoles of solute per liter of solution
In the body, were generally measuring milliosmoles
Osmolality
Omsoles of solute per kilogram of solvent
Osmolarity vs osmolality
They are NOT interchangeable but since we are looking at the relative differences, we can use either as long as were consistent with our terms
For dilute solutions, the difference between osmolarity and osmolality is insignificant
Where do nephrons create an osmotic gradient
Within the renal medulla
Long nephron loops and the gradient
The long nephron loops of juxtamedullary nephrons create the gradient
Act as countercurrent multipliers
The countercurrent multiplier depends on three properties of the nephron loop to establish the osmotic gradient
- Filtrate flows in the opposite direction (countercurent) through the two adjacent parallel sections of a nephron loop
- The descending limb is permeable to water, but not to salt
- The ascending limb is impermeable to water, and pumps out salt
Positive feedback cycle that uses the flow of fluid to multiply the power of the salt pumps
- Salt is pumped out of the ascending limb
- Increase in intestinal fluid osmolality
- Water leaves the descending limb
- Increase in osmolality of filtrate in descending limb
- Increase in osmolality of filtrate entering the ascending limb
Vasa recta and the gradient
The vasa recta preserves the gradient and they act as countercurrent exchangers.
Collecting ducts
use the gradient to adjust urine osmolality
Cycle of water and solutes
(As water and solutes are reabsorbed, the loop first concentrates the filtrate, then dilutes it)
- Filtrate entering the nephron loop is isosmotic to both blood plasma and cortical interstitial fluid
- Water moves out of the filtrate in the descending limb down its osmotic gradient. This concentrates the filtrate
- Filtrate reaches its highest concentration at the bend of the loop
- Na+ and Cl- are pumped out of the filtrate. This increases the interstitial fluid osmolality
- Filtrate is at its most dilute as it leaves the nephron loop. At 100 mOsm, it is hypo-osmotic to the interstitial fluid
Glomerular filtration rate
amount of filtrate produced per minute
Average: 125 mL/minute
GFR is based on three pressures present in glomerulus
Blood hydrostatic pressure (BHP), colloid osmotic pressure (COP), and capsular pressure (CP)
Blood hydrostatic pressure (BHP)
Blood pressure in the glomerulus (out)
Colloid osmotic pressure (COP)
Pressure exerted by proteins in the blood (in)
Capsular pressure (CP)
Pressure exerted by filtrate in the glomerular capsule (in)
Blood pressure and GFR
- Adequate blood pressure (BHP) is required to maintain GFR (Nephron action can alter blood volume, thereby altering pressure)
- GFR needs to be controlled or can lead to kidney failure
Too high GFR
Excessive urination, damage to kidneys
Too low GFR
Inadequate filtration, build up of toxins
How is resting homeostasis in healthy humans maintained when GFR is too high
Too high from blood pressure
Cardio/vasomotor mechanisms try to lower blood pressure/GFR
How is resting homeostasis in healthy humans maintained when GFR is too low
From low blood pressure
Cardio/vasomotor mechanisms try to raise blood pressure/GFR
Hormonal regulation
Hormones
Hormones are chemicals in the body that cause changes to other tissues in the body
What are the different hormones involved in raising GFR when blood pressure is low
- Renin and angiotensin (these work together)
- Aldosterone (The salt hormone)
- Antidiuretic Hormone (ADH)
Where is the juxtaglomerular apparatus (JGA) located
At the junction of the DCT and afferent arteriole
Juxtaglomerular apparatus (JGA)
Cells that monitor and adjust GFR
Consists of Juxtaglomerular (JG) cells and Macula densa cells
Juxtaglomerular (JG) cells
- In the afferent arteriole (blood vessel)
- Secrete renin in response to signal rom macula densa cells
Macula densa cells
- In the distal convoluted tubule (nephron)
- Monitor urine in DCT and tell JG cells how fast the urine is moving
How do macula densa cells work
- When GFR decreases, filtrate moves more slowly through the nephron
- The slower movement of filtrate causes more NaCl to be reabsorbed into the blood from the nephron loop
- The filtrate then becomes more dilute compared to normal (because NaCl has moved out)
- Macula densa cells detect the dilute filtrate and respond by triggering JG cells to release renin
Hormonal regulation in response to low blood pressure
- Renin released by JG cells
- Renin activates a protein called angiotensinogen in blood which is a precursor to angiotensin I
- Angiotensin I is activated to angiotensin II by ACE, primarily in the lungs
Angiotensin II
- Results in increased blood pressure
- Widespread vasoconstriction in body
- Stimulates thirst (target hypothalamus)
- Stimulates secretion of aldosterone
- –Stimulates reabsorption of sodium ions in the DCT and collecting duct
- –Water follows because of osmosis, more water in blood increases pressure
- Stimulates secretion of antidiuretic hormone (ADH)
- –More water reabsorption
Antidiuretic hormone (ADH)
- Produced by hypothalamus in response to dehydration
- Causes the production of aquaporins in collecting duct
- Allows for uptake of water faster
- Production of aquaporins decreases as rehydration occurs
- Alcohol blocks ADH production
