Renal: Regulation of Body Water Volume, Osmolarity and Ions Flashcards
key mechanisms regulation Na and Water excretion/retention (brief steps, which ones are direct vs hormonal)
1) Glomerulotubular Balance
2) Pressure Natiuresis
3) Antidiuretic Hormone (ADH)/Vasopressin
4) Renin-Angiotensin-Aldosterone System
5) Atrial Natiuretic Peptide
1 and 2 are direct (intrinsic) renal mechanisms, 3, 4 and 5 are hormonal
(systemic)
direct regulation of Na levels; glomerularlotubular balance (what is it, consequences, summary)
Glomerulotubular balance (GTB) is defined as the ability of each successive segment of the proximal
tubule to reabsorb a constant fraction of glomerular filtrate and solutes delivered to it.
Consequently, when too much Na+ is present, plasma volume and renal
blood flow rise and GFR increases. Since only a fixed fraction of that Na+ can be reabsorbed, a higher total amount of Na + remains in the tubule (the fraction is the same, but because the volume is higher, there is actually more Na+ remaining in the fluid). This ultimately passes out in the urine and is lost, leading to a decrease over time in Na+ and normalization of blood volume
high vascular volume -> GFR inc -> kidney takes out fraction -> rest of Na goes through and leaves in urine
(amt in urine increases if you consume more salt)
steps for glomerulotubular balance
change in body sodium level -> change in water “retained” -> change in blood volume -> change in bloodflow/GFR -> change in sodium excretion (goes back to change in body sodium level)
what is pressure natiuresis
Pressure changes in the vascular system of the kidney directly alter sodium excretion. This is complicated and is called “pressure natriuresis” (this is over and above glomerulotubular balance – you don’t need to know the mechanism).
sensing and regulation of plasma and ECF osmolarity
- Changes in plasma or ECF Osmolarity as little as 3 mOsm/kg trigger changes in the size of osmoreceptor neurons in the hypothalamus.
- Change in cell size alter the release of ADH/ Vasopressin (shrinkage of cells due to ECF hyperosmolarity increases release and vice versa)
- ADH increases water reabsorption by kidney and stimulates thirst
steps for hormonal regulation of water balance: ADH
- plasma osmolality increases
- ADH hormone released
- binds with V2 receptor (in CD)
- water reabsorbed back into circulation
plasma osmolarity; sensed parameter, sensor mechanism, effector (hormones), systems affected/altered)
sensed parameter = blood solute concentration
sensory mechanism = osmoreceptors (brain)
effector = ADH
systems affected/altered = urinary h20, thirst/h20 intake
ECF volume regulation; effective circulating volume
- There is a set point of “fullness” which correlates with the pressure at different points within the vascular system (related to the physical
capacity of the vascular system to hold the blood at an appropriate
pressure). - In healthy animals this is directly proportional to ECF volume (which depends on the total body Na+ content) and other factors like heart
function and oncotic pressure - In some pathophysiologic states there is an expanded ECF volume
but a decreased effective circulating volume – hypoproteinemia, edema, etc. – Meaning the body is retaining fluid, but that it isn’t contributing to circulation
regulation of Na balance (steps)
effective circulating volume -> volume sensors -> kidneys -> alteration in NaCl excretion (circles back to effective circulating volume)
blood volume ; sensed parameter, sensor mechanism, effector (hormones), systems affected/altered
sensed parameter = effective vascular (circulating) volume
sensor mechanism = stretch receptors (heart, lungs, carotid, kidney)
effector (hormones) = ANP (from heart), ANGII (via renin), aldosterone (via ANGII)
systems affected/altered = urine Na excretion (ANP increases excretion, aldo decreases excretion)
vascular volume sensors; location
- Low-pressure mechanoreceptors (volume receptors)
– Lead to changes in Atrial Natriuretic Peptide (ANP)
– Cardiac atria and pulmonary vessels - High-pressure baroreceptors (pressure receptors)
– Aortic arch, carotid sinus
– Lead to changes in autonomic outflow (norepinepherine) which affects blood pressure, renin and angiotensin (II) levels - Kidney
– Juxtaglomerular apparatus (granular cells) and renal visceral
afferent nerves
– Lead to changes in renin release which alters angiotensin (II) levels.
volume sensors in atria; atrial natriuretic peptide
A potent polypeptide released by cells in the atrial wall in response to stretch. Decreases blood pressure/volume by eliminating more sodium (and causing other hormonal changes). Water follows the sodium and ECV is decreased
atrial natriuretic peptide (ANP), details and what happens overall
- Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole (increases GFR and Na excretion)
- Decreases sodium reabsorption in the distal tubule and cortical collecting duct (increases Na excretion)
- Increases blood flow through the vasa recta which will carry more solutes (NaCl and urea) out of the medullary interstitium.
- Decreased osmolarity of the medullary interstitum leads to increased fluid excretion (system is less able to reabsorb water – water is excreted)
- ANP directly decreases renin secretion.
- ANP directly decreases aldosterone secretion.
Overall effect is to decrease ECV when ANP is released and increase ECV when ANP levels are low
Second Volume/Pressure Sensor: Renin-Angiotensin-Aldosterone system
If blood pressure decreases, renin release is stimulated due to:
* Reduced renal perfusion pressure (pressure sensors in JG apparatus of kidney)
* ↑ Sympathetic activity (high pressure receptors in carotid and aorta)
– norepinepherine stimulates renin release.
* ↓Delivery of NaCl to macula densa cells stimulates renin release
renin-angiotensin-aldosterone system
- Increased renin ultimately leads to increased angiotensin II levels, which increases aldosterone secretion by adrenal cortex.
- Also stimulates additional ADH secretion by hypothalamus. Overall effect is an increase in sodium, then an increase in ECV when a drop in pressure/volume is sensed. Opposite effects (decreased sodium, decreased ECV) occur when a pressure increase is sensed
