Osmotic and Volume Regulation (B2: W5) Flashcards
How do chages in volume affect ADH release?
E.g. Hemorrhage
- Plasma volume goes down, so vascular pressure drops
- Reflexes mediated by cardiovascular baroreceptors send a message
-
ADH release increases
- Plasma ADH goes up
- Tubular permeability to water goes up
- Water is reabsorbed
How does the body respond to the consumption of 1 liter of saline?
- Extracellular fluid goes up
-
ADH release goes down
- Water is excreted
- Plasma osmolarity increases
- ADH increases
Initially ADH goes down, but eventually is increased again
How does the body respond to the consumption of 1 liter of distilled water?
- Plasma osmolarity decreases
- ADH is decreased
- Want to raise Posm
- Water is excreted
How is extracellular fluid volume regulated?
By regulating sodium reabsorption
Where is sodium reabsorbed along the neprhon?
- 67% reabsorbed in the proximal tubule
- More is reabsorbed in the ascending limb
- 8% remaining
- Additional reabsorption in distal tubule, convoluted collecting tubule, and collecting duct
- 0.5% is usually excreted
When juxtaglomerular cells sense less stretch, they release ______.
Renin
What factors are associated with moving sodium back into the body to control extracellular fluid volume?
Kidney is in control of sodium retention
Affected by
- GFR
- Aldosterone
- Natriuretic hormone
- Peritubular pressure
When regulating volume, which is regulated first: sodium or water?
Regulation of volume requires first regulating sodium followed by regulating water
What is the relationship between filtered load and sodium reabsorption in the proximal tubule?
As the filtered load of Na goes up, a constant proporiton is reabsorbed in the proximal tubule - 67%
- In the case of hypovolemia
- Shifts graph to be more efficient and save salt
- Slope goes up - maybe 69% instead
- In the case of hypervolemia
- Slope goes down and less salt is saved
Why does excess sodium consumption lead to an increase in extracellular fluid volume?
- Plasma [Na] goes up
- Plasma osmolarity increases
- Shifts water from inside of cells OUT
- Increase ADH to save water
- Water reabsorption and consumption
- Extracellular volume increases again
This process is slower than just drinking water
How does aldosterone affect collecting duct principal cells?
- Aldosterone released in response to BP decrease (Angiotensin II) or in response to hyperkalemia
- Aldosterone gets into cell to intracellular receptor where it affects the synthesis of proteins
- Makes more Na channels
- Enhances ATP generation
- Makes more Na/K ATPases
How does aldosterone affect hydrogen atoms?
Enhances H+ secretion in the collecting duct
- Becomes more acidic
- More Na is reabsorbed back into the body
What are the two primary regulators of aldosterone release?
- Increased angiotensin II
- Increased plasma potassium concentration
Two minor regulators that are not as important
What three effects does aldosterone have on the kidneys?
- Increased Na reabsorption
- Increased K excretion
- Increased H excretion
What are the effects of hypoaldosteronemia (e.g. adrenal insufficiency - Addison’s disease)?
- Acidosis
- Hyperkalemia
- Hypotensin (salt wasting)
What are the effects of hyperaldosteronemia?
- Alkalosis
- Hypokalemia
- Hypertension (usually not overt volume expansion
What are the two types of hyperaldosteronemia, and what distinguishes the two?
- Primary: producing too much aldosterone
- Tumor
- Hypetension
- Renin release is decreased - more stretch
- Secondary: something else caused aldosterone to increase
- Renal artery stenosis
- Renin release is increased - less stretch
Both are associated with hypertension
What effect does Atrial Natriuretic Factor have on aldosterone?
ANF is the “anti-aldosterone”
- Released under opposite conditions - atrial stretch (increased volume)
- Acts via membrane receptors coupled to guanylate cyclase
- Decrease in sodium reabsorption in the collecting duct
- Increase in GFR
- Decrease effects of renin, angiotensin II, and aldosterone
What is natriuresis?
Excretion of excess sodium in the urine
What is the main regulator for sodium handling in the kidneys?
Arterial baroreceptors maintain effective cirulating volume (ECV - in the arterial system)
Why do patients with heart failure exhibit markedly positive and progressively increasing sodium balance?
Baroreceptors in arteries sense a drop in the volume and save sodium, which in turn saves water
- Shift in volume to venous system is sensed as a decreased volume
- Message to kidneys: save more sodium
What are the stages of kidney disease?
- Stage 1: kidney damage with normal or increased kidney function
- Stage 2: kidney damage with mild decreased kidney function
- Stage 3: moderate decreased kidney function
- Stage 4: severe decreased kidney function
- Stage 5: kidney failure
- GFR ~15
How do you keep sodium reabsorption the same, even with fewer nephrons?
- Losing GFR and filtered load
- Matched by increased fractional excretion of sodium
- Remaining nephrons dump more sodium out
- Normally, 0.6% excreted
- With 1/10 the amount of functioning nephrons, 6% excreted
What happens to plasma and urine chemistry with nephron loss?
- Patient becomes more acidotic with progressive loss of nephrons
- Plasma creatinine and BUN increase
- These are produced every day - must go out in kidneys
- With fewer nephrons, less can leave
How can a patient remain in creatinine balance with progressive nephron loss?
- 1 mg/min produced every day
- Need to excrete this amount per day in nephrons
- 10 times as much in each mL
- Can get 1/10 of the nephrons to excrete what we need
What stimulates the kidneys to generate and release erythropoietin?
Reduced tissue oxygenation
