Lecture 33 - Body water, distribution and regulation of body water Flashcards
What drives and regulates body water homeostasis?
Distribution of body water Osmolarity/tonicity of solutions Reabsorption of water in the nephron Changes in body osmolarity Effects of osmotic changes in the kidney
Ultimate goal is to maintain blood pressure in the body and control it
Distribution of body water
TBW is 55% (female) - 60% (male)
ECF = 1/3TBW
ICF = 2/3TBW
Plasma = 1/5 of EcF
Interstitial fluid = 4/5 of ECF (this is the fluid between cells)
Osmolarity
Based on the number of osmotically active ions or solutes
145mM NaCl = 145 mM Na+ + 145 mM Cl- = 290 mosmol/L
Can be estimated by specific gravity (the density of solutions) - Specific gravity is just an estimate of osmolarity because specific gravity measures the density of solutions rather than the osmotic activity of the solutions
Tonicity
Based on the effect of a solutions on cells
An isotonic solution does NOT change water homeostasis between cells
Isosmotic
Same osmolarity
Hyposmotic
Lower osmolarity
Hyperosmotic
Higher osmolarity
Composition of ECF and ICF/ body water balance
Na+ is higher in the ECF than ICF
K+ is lower in the ECF than the ICF
Intake (water in food, ingested fluid and water formed by catabolism) = Output (lungs, skin by diffusion, skin by sweat, kidneys urine, intestines in faeces)
Total body water remains relatively constant (main reason is for the maintenance of blood pressure)
Intake and loss of water must balance
Urine output is adjusted to maintain balance
Reabsorption of sodium
Uses sodium - Main driver for water reabsorption is sodium which comes first so the sodium-potassium ATPase sets up a gradient and then results in water following
There are 4 important places within the nephron where sodium (filtered load) is reabsorbed - PCT (67%), TAL (25%), DCT (5%), CD (3%)
Urinary excretion of Na+ = 0.5-1% of the filtered load (99% of the sodium foes back into our system for blood pressure control)
Reabsorption of water
There are 3 important places within the nephron, where water is reabsorbed - PCT (67?), tDLH (25%), CD (2-8%)
Urinary excretion of water = 0.5-8% of filtered load
Normal secretion under normal conditions would roughly be 0.5-1% again but this variation in the urinary excretion of water is based on how much water we take in and how much we need to take out to keep blood pressure constant, the collecting duct responds to changes in drinking by changing the osmolarity of the plasma
Reabsorption of water - PCT
PCT main function is bulk reabsorption
Water reabsorption in the PCT (67% of the filtered load) is driven by Na+ reabsorption (isosmotic)
Water reabsorption is facilitates by aquaporins (trans-cellular) and via leaky tight junctions (paracellular)
Na+-K+ ATPase is the main driving enzyme which requires energy to do its job so that it keeps the sodium concentration inside cells low
Sodium gradient is used by sodium glucose transporter to drive water reabstoption and this is the same mechanism as what is happening in the intestine
Process of the reabsorption of water in the PCT in terms of sodium
From the filtrate in the tubular lumen, the Na+ will flow down its concentration gradient into the tubular epithelial cells
It will then be actively transported via the Na+/K+ ATPase pump to the interstitial fluid
This increases the osmolarity of the interstitial fluid, which creates an osmotic gradient, meaning water will move into the interstitial fluid
THis reabsorption of water can happen both paracellularly (through leaky tight junctions) and transcellularly ( via aquaporins in the cell membrane)
The water in the interstitial fluid will then move via bulk flow into the peritubular capillaries
Bulk flow is a passive process driven by the hydrostatic and osmotic pressure gradients
Reabsorption of water - nephron loop
The TAL reabsorbs Na+ into the interstitial generating a High Osmotic Medullary Gradient (HOMG); the tDL is leaky epithelium facilitated water reabsorption via aquaporins (transcellular) and the paracellular pathway
The reabsorption of water in the loop of henle works in a counter current mechanism
The thin DLH is highly permeable to water because it has leaky epithelium allowing water to move through both paracellular (leaky tight junctions) and transcellular (aquaporin) methods
The tDLH is impermeable to solutes/ions so how does water move?
There is a osmotic gradient created by the thick ascending loop as it contains lots of channels/pumps allowing for ions (Na+ and Cl-) to be reabsorbed into the interstitium
This creates a hyper osmotic interstitum in the medulla and drives water reabsorption from the tDL
Thick ascending limb
Impermeable to water
Selectively permeable to Na+ and Cl-
Solute concentration decreases
Thin descending limb
Permeable to water
Impermeable to solutes
Solute concentration increase
True of false - the reabsorption of water in the nephron loop is to the same extent as sodium reabsorption
True
Changes in body osmolarity
Changing water content changes osmolarity
FLuid shifts between the ECF and ICF to equalise - dependent on how much water intake you have
Volume o compartments change i.e. changing water content changes cell size which means that sell structure is altered and that cell functions can become impaired
ICF/ECF have the same osmolarity (275-295 mosmol/L) because water moves freely between the two compartments and if one area has a high osmolarity, water will move until equilibrium is reached
THe problem is that the compartment that the water moves into will increase the volume
This means that we need to regulate the water, to regulate the osmolarity to regulate the cell size as you do not want to overfill them
So we can regulate our water input by drinking or not drinking (regulate osmolarity in order to regulate cell size)
Hypertonic
Higher solute concentration outside the cell so water rushes out, cell shrivels
Hypotonic
Higher solute concentration inside of the cell so water rushes in and causes the cell to swell
Isotonic
Red blood cells are dependent on an isotonic environment
Contains equal concentrations of solute so the cell neither swells or shrinks
Dehydration and changes in body osmolarity
Not drinking - water lost (only) from the ECF
ECF osmolarity increases to approx 320 mosmol/L (ECF gets more concentrated)
Now there is a difference between - ECF = 320 mosomol/L vs ICF= 285 mosmol/L
Water moves to higher osmolarity
From ICF (cells) to ECF until osmolarity is balanced
But cells will become smaller
ECF osmolarity has to be controlled
Hyperhydration and changes in body osmolarity
Excess drinking - water gained (only) by the ECF
ECF osmolarity decreases to approximately 240 mosomol/L
Now difference is ECF=240 vs ICF=285
Water moves to higher osmolarity
From ECF to ICF (cells) until balanced
But cells will become bigger
ECF osmolarity has to be controlled
Regulation with ADH of changes in body osmolarity
Total body water changes alter plasma (ECF) osmolarity….
Detected by osmoreceptors in the hypothalamus (brain)
Stimulates pituitary gland to secrete more/less ADH
ADH alters permeability of renal collecting duct (CD)
So water retained/excreted to balance initial change in TBW
- Plasma osmolarity stable
- Cell volume is stable
ADH function
ADH is a hormone that helps the body to retain water by increasing water reabsorption by the kidneys
Hormone from the posterior pituitary
ADH synthesis
In the cell body of central neutrons in the hypothalamus. Then axonal transport to posterior pituitary
ADH release
It is in the posterior pituitary and is then released into the bloodstream (neurosecretion)
Two major stimuli for ADH release
Increased ECF osmolarity
Decreased blood volume
Actions of ADH
Inserts water channels called aquaporins in luminal membrane of the collecting duct
Increase water reabsorption in the collecting duct
Obligatory water reabsorption
Not regulated
Accounts for 92% of total water reabsorption
Glomerulus and PCT and descending part of the nephron loop
The amount of water reabsorbed in the kidneys regardless of a person’s state of hydration.
Facultative water reabsorption
Tight epithelia
Only transcellular
Regulated by ADH
Accounts for 2-8% of total water reabsorption
Occurs in the distal convoluted tubule and the collecting duct
Dependent on hydration status
With ADH water reabsorption
Antidiuretic hormone binds to receptors on cells in the collecting ducts of the kidney and promotes reabsorption of water back into the circulation. In the absense of antidiuretic hormone, the collecting ducts are virtually impermiable to water, and it flows out as urine.
Small volume of concentrated urine
Antidiuresis
Means that you can reabsorb water from the collecting duct
Without ADH water reabsorption
ADH causes the insertion of water channels into the membranes of cells lining the collecting ducts, allowing water reabsorption to occur. Without ADH, little water is reabsorbed in the collecting ducts and dilute urine is excreted.
Therefore large volume in dilute urine
Diuresis
Cannot reabsorb water from the collecting duct - flush out whatever is in the urine because the collecting duct is tight for water
Diuresis
Increased or excessive production of urine
Antidiuresis
reduction in or suppression of the excretion of urine.
Mechanism of ADH effect
ADH in the bloodstream finds its receptor on the basolateral side of the collecting duct receptors
ADH via intracellular signaling cascades increases the number of aquaporins in the apical membrane increasing water permeability of the apical membrane
Urine osmolarity is
Controlled by the pituitary glands
