Flashcards in Lecture 18: Integration salt and water balance 2 Deck (31):
Where is aldosterone released from?
- zona glomerulosa cells of the adrenal Cortex
Where is ACE released from?
Where is angiotensinogen released from?
What causes aldosterone release?
1. Most powerful: K+ conc (ECF)
2. Angiotensin II
Aldosterone action cellularily
1. Aldosterone binds to non-specific MC mineralocorticoid receptor from intersitial side (spironolactone competitive inhibition)
2. events in nucleus
3. ENac channel causes increased sodium reabsorption into cell
4. Na finally pushed into ECF via NaK ATPase
5. Decreased potassium levels
What competitively inhibits MC receptor on interstitial side?
What competitively inhibits ENaC channel on tubular lumen side?
- K sparing diuretic
Normally aldosterone stimulates the reabsorption of 33g of NaCl daily.
If patient loses 10% adrenal function --> will 33g of NaCl be excreted per day indefinitely?
System has compensation/redundancy: if there is an inappropriate angiotensin of aldosterone response --> there is enough backup to continue (even though not being as ideal)
Sodium loss --> stimulates Na retention mechanisms --> adrenal gland cortex failure results in inability to secrete aldosterone
Other factors will continue to try --> decrease GFR --> increased Na reabsorption (partially)
Regulation of ecf Osmolality
osmolality = tightly controlled = changes in ions
- REGULATED by H2O handling
- Mediator: ADH
Regulation of ecf Volume
fluid volume = quanitity of water
- REGULATED by Na handling, as it drives water movement
- varies alot around the day -> therefore need lots of backup mechanisms (surrounding Na movement) to control ecf Volume
Out of ecf osmolality and volume what varies more and what does this mean re its regulators?
1. ecf Volume varies throughout the day
--> this means that it requires More Regulator mechanisms (surrounding Na movement) to control its fluctuations
Why do you want to keep osmolality within tight range?
Brain cells dont like changes in osmolality
hyper/hypo osmolality --> nausea, headaches, confusion, lethargy, weakness, seizures
Attempted suicide with soy sauce
Massive change in blood volume
All fluid has come out to try balance osmolality
- high Na in blood -->
- ADH levels decreased
- Renin decreased --> decreased reabsorption of Na
- small increase in Blood volume
Hyponatremia in marathon runners
Historical advice: continually drink water
13% of runners had Hyponatremia (over hydrated)
What happens when there is a High ECF volume?
Decreased reabsorption of Na
- as Na regulates ECF volume levels
What increases Na reabsorption?
What decreases NA reabsorption?
2. Decreased RAAS and SNS
released from heart in response to increased Pressure and Stretch on heart
What are the actions of ANP
1. Blocks ENac + Inhibits NaKATPase --> decrease DT Na reabsorption
2. Inhibits aldosterone release
3. Inhibits renin release
4. Vasodilates afferent arteriole --> increased GFR
5. Urodilation released by kidney (30 aa almost identical to ANP)
6. Dopamine released by PT neurons --> inhibition of PT NaKATPase and NaH exchanger
primarily negative feedback loops
What are the 2x regulators of osmolality?
Osmolality is regulated by water change
1. osmorecetpors --> ADH from kidney
2. thirst --> brain/drinking behavior
-- NEgative feed back
What are the sensors and regulators of blood pressure changes?
Blood pressure: carotid sinus + aortic arch baroreceptors
Blood volume: atrial stretch receptors
- Short term : BP
- long term: NA secretion
What happens during dehydration?
What happens when you eat alot of salty chips?
Step 1: Increased osmolarity --> decrease in osmalarity via increase in ECF
Step 2: Increased ECF --> excrete (slow) + rapid (blood pressure changes CVCC ANS)
What is the relationship b/w SNS and Na levels
Increased Na levels --> decrease SNS activity --> decreases Volume
What is the relationship b/w change in SNS and change in Blood PRessure
Even if Blood pressure doesn't change
- SNS activity will change renal 1. RAAS system independently 2. vasoconstriction of afferent arteriole --> changes GFR (extrinsic mechanisms)
What is the impact of a high salt pasta meal re angiotensin?
- high salt = high volume = decrease RAAS
Decreased angiotensin II --> decreased aldosterone --> decreased Na reabsorption
Dehydrations relationship with ADH
What is the angiotensin response to hemorrhage if renal nerves to the kidney are denervated?
- hemorrhage --> decrease BP --> reduction in afferent arteriolar --> increased SNS
Effects of increasing angiotensin II on salt and water in urine
Increased angiotensin II --> Increased reabsorption of Na and hence water --> decreased Na and water in urine