Sodium ad water reabsorption, control of body water and urine consumption Flashcards
Describe water reabsorption (where and they types) in the nephron
There are three important places where water is reabsorbed in the nephron:
- PCT: 67% of filtered load reabsorbed
- deciding limb of nephron loop: 25% of filtered load reabsorbed
- CD: 2-8% of filtered load reabsorbed
- Excretion: <1-6% of filtered load is excreted
Bulk (obligatory) water reabsorption:
- occurs in the PCT and depending nephron loop
- accounts for 92% of total water reabsorption
- not regulated - automatic!
- leaky epithelia
- trans- and paracellular water reabsorption
Regulates (facultative) water reabsorption:
- occurs in the CD
- accounts for 2-8% of total water reabsorption
- regulated by anti-diuretic hormone (ADH)
- tight epithelia
- only transcellular reabsorption
describe sodium reabsorption (where and types) in the nephron
There are four important places where sodium is reabsorbed in the nephron:
- PCT: 67% of filtered land reabsorbed
- ascending limb of the nephron loop: 25% of filtered load reabsorbed
- DCT: 5% of filtered load reabsorbed
- CD: 2-3% of filtered load reabsorbed
- excretion: <1% of filtered load is excreted
Bulk sodium reabsorbtion:
- accounts for 92% of total sodium reabsorption
Regulated sodium reabsorption:
- accounts for 7-8% of total sodium reabsorption
- regulated by aldosterone (RAAS)
what drives and regulates body water homeostasis?
- distribution of body water
- osmolarity of solutions
- changes in blood osmolarity
- reabsorption of water and sodium in the nephron
- effects of osmotic changes on the kidney
- effects of volume changes on the kidney
describe reabsorption in the PCT
- water reabsorption in the proximal tubule (67% of filtered load) is driven by Na+ reabsorption (isosmotic!!)
- transporters such as the sodium-glucose cotransporter use the sodium gradient to reabsorb solutes (like glucose) - on the apical membrane
- glucose and sodium are transported through the proximal tubule cells
The proximal tubule is ‘leaky; epithelia. the strong electrochemical gradient pulls other things through to balance:
- chloride follows via the paracellular pathway (pulled towards the positive charge of K+ and Na+)
- water follows by the paracellular (between the cells) and the transcellular (across cells) pathways due to the change in osmolarity (osmotic gradient)
describe reabsorption in the nephron loop
Descending: permeable to water
Ascending: permeable to sodium
(water flows downhill)
- the descending loop is leaky epithelium, so water is reabsorbed from the nephron into the peritubular fluid.
- via the transcellular pathway: aquaporins and via the paracellular pathway, across the junctions between cells
- the ascending loop reabsorbs Na+ into the peritubular fluid
describe the juxdamedullary nephrons reabsorption in the nephron loop
the different permeabilities of the decending (water) and ascending (sodium) parts of the JMNs loop allows them to generate a hyper-osmotic medullary gradient (HOMG).
The deeper you go in the medulla, the higher the osmolarity is
describe reabsorption in the DCT and collecting duct (for water and sodium)
Water: collecting duct
- regulated water reabsorption
- tight epithelia
- only transcellular reabsorption
- regulated by anti-diuretic hormone (ADH)
Sodium: DCT and CD
- regulated sodium reabosrption
- regulated by aldosterone (RAAS)
describe the regulation of body osmolarity via ADH
TBW changes alter plasma (ECF) osmolarity
- detected by osmoreceptors in hypothalamus
- stimulates posterior pituitary gland to secrete more/kess ADH
- ADH alters permeability of collecting duct cells, so water is retained/excreted to balance the initial chance in TBW
- plasma osmolarity stable
- cell volume stable
Increasing osmolarity (Na+ levels) in ECF:
- ADH secretion increases
- effector: kidney
- water reabsorption by kidneys increases and thirst promotes water consumption
- ECF volume increases due to the gain of water. causing the osmolarity (and Na+) to decrease
- homeostasis restored by decreasing osmolarity in the ECF
Decreasing osmolarity (Na+ levels) in ECF:
- ADH secretion decreases
- effector: kidney
- water loss by kidney increases and thirst is suppressed
- ECF volume decreases due to the loss of water. causing the osmolarity (and Na+) to increase.
- homeostasis restored by increasing osmolarity in the ECF
describe the regulation of body osmolarity using ADH when there is a decrease in TBW
- TBW decreases
- increase in ECF osmolarity
- detected by osmoreceptors in the hypothalamus
- increase of ADH from the posterior pituitary
- insertion of aquaporins in apical membrane of CD cells once their receptors sense ADH: which increases water permeability (the aquaporins are stored inside the epithelial cells in storage membranes, which join onto cell membrane when ADH triggers cells)
- increase in water reabsorption and decrease in urine volume
- ECF osmolarity returns to normal
describe the reabsorption of water in the nephron in the collecting duct
with ADH the reabsorption of water in the collecting duct is way larger. The driving force for this to occur is the hyper-osmotic medullary gradient that is produced in the juxtamedullary nephrons. This will always be there in a healthy kidney.
- so the aquaporins are the pathway, and the gradient made by the HOMG is the driving force
describe the regulation of ECF volume - using aldosterone and ANP
Changes in ECF volume:
- increase in volume: ANP
- decrease in volume: aldosterone (RAAS)
Increasing ECF volume by fluid and Na+ gain:
- receptors: cardiac muscle cells
- release of ANP
- effectors: kidneys
- increased Na+ and water loss in urine
- homeostasis restored by decreasing ECF volume
Decreasing ECF volume by fluid and Na+ loss (eg. vomiting, blood loss, diarrhoea)
- receptors: kindyes
- endocrine response of the kidneys: actuate RAAS leading to increased release of aldosterone
- increased ADH release
- decreased Na+ and water loss in urine
Remember: gain or loss of isosmotic fluid only affects the ECF
describe the regulation of ECF volume using aldosterone (RAAS) for decrease in blood volume/loss of isosmotic fluid (water and Na+)
- decrease in blood volume/loss of isosmotic fluid
- detected by pressure receptors in the kidney
- activation of RAAS, increased release of aldosterone from the adrenal gland
- increased sodium channels in apical membrane of DCT and CD (sodium channels stored inside epithelial cells, when aldosterone binds, these channels are taken to the apical surface of the cells)
- increased sodium and water reabsorption (water follows the sodium via the aquaporins, same as before)
- blood volume returns to normal
describe the normal and pathological composition of urine
Normal:
- water: 96-98% of urine is water (1.5L/day)
- creatinine (muscle metabolism)
- urea (amino acid breakdown)
- uric acid (purine breakdown)
- H+ (hydrogen ions)
- Na+ (sodium), K+ (potassium)
- Medications (anti-viral, diuretics)
- toxins
Pathological:
- glucose (glucoseuria, diabetes)
- protein, especially albumin (proteinuria)
- blood: RBCs/erythrocytes (haemoturia)
- haemoglobin (haemotogblinuria)
- white blood cells/leucocytes
- bacteria (infection)
what can you see, taste or smell in normal vs. pathological urine?
Normal urine:
See: clear, to light or dark amber
Taste: pH dependant on diet
- average person: pH of 6-7.5
- vegetarians: pH of up to 8
- high protein diet: pH as low as 4.6
Small: unremarkable
Pathological urine:
See: orange, red, brown, blue/green
Taste:
- sweet: diabetes mellitus
Smell:
- ‘fruity’ ketones from: gasting, diabetes, or chronic alcohol abuse
- ‘rotten’: infection (bacteria), tumour
