Lecture 18: Integration salt and water balance 2 Flashcards
Where is aldosterone released from?
Adrenal gland
- zona glomerulosa cells of the adrenal Cortex
Where is ACE released from?
lungs
Where is angiotensinogen released from?
Liver
What causes aldosterone release?
- Most powerful: K+ conc (ECF)
2. Angiotensin II
Aldosterone action cellularily
- Aldosterone binds to non-specific MC mineralocorticoid receptor from intersitial side (spironolactone competitive inhibition)
- events in nucleus
- ENac channel causes increased sodium reabsorption into cell
- Na finally pushed into ECF via NaK ATPase
- Decreased potassium levels
What competitively inhibits MC receptor on interstitial side?
Spirolactone
What competitively inhibits ENaC channel on tubular lumen side?
Amiloride
- 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
- -> Mediators:
1. RAAS
2. SNS
Out of ecf osmolality and volume what varies more and what does this mean re its regulators?
- ecf Volume varies throughout the day
- -> this means that it requires More Regulator mechanisms (surrounding Na movement) to control its fluctuations - RAAS
- SNS
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?
- RAAS
- SNS
- ADH
- SNS
What decreases NA reabsorption?
- ANP
- Decreased RAAS and SNS
- dopamine
- prostaglandins
- ANP
ANP
released from heart in response to increased Pressure and Stretch on heart
28 aa
What are the actions of ANP
- Blocks ENac + Inhibits NaKATPase –> decrease DT Na reabsorption
- Inhibits aldosterone release
- Inhibits renin release
- Vasodilates afferent arteriole –> increased GFR
- Urodilation released by kidney (30 aa almost identical to ANP)
- Dopamine released by PT neurons –> inhibition of PT NaKATPase and NaH exchanger
Diagram**
Homeostatic regulation
primarily negative feedback loops
What are the 2x regulators of osmolality?
Osmolality is regulated by water change
- osmorecetpors –> ADH from kidney
- 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 Kidney effector - Short term : BP - long term: NA secretion
What happens during dehydration?
Sensors: Signals: Effectors: Eventual response: Diagram**
What happens when you eat alot of salty chips?
Sensors:
Signals:
Effectors:
Eventual response:
Diagram**
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
Increased 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
What is the relationship b/w stenosis of the renal artery and sodium and water rebsorption
Stenosis of renal artery –> decreased flow into kidney –> increased water and sodium reabsorption
