Flashcards in Lecture 17 Deck (25):
Where is aldosterone released from?
Adrenal gland - cortex.
What will increase the release of aldosterone?
Angiotensin 2 and extracellular potassium concentrations.
What does aldosterone bind to in the kidney?
It binds to mineralocorticoid receptors on the principal cells of the cortical collecting tubule.
What happens when aldosterone binds to principal cells?
An ENaC channel is formed, it allows sodium to be reabsorbed, the sodium will be pushed into the capillary space by the Na/K/ATPase, so you then get secretion of potassium. That is why high potassium levels will cause an increase in aldosterone levels.
What drugs block aldosterone?
Spironolactone. This binds to the mineralocorticoid receptor. The ENaC channel can be blocked by amiloride (diuretic).
Describe essential hypertension?
it is estimated that up to 10% of essential hypertension may have hyperaldosteronism (increase in aldosterone levels). You can treat this by spironolactone.
Normally aldosterone stimulates the reabsorption of approx. 33g of sodium chloride/day. if a patient loses 100% of adrenal function, will 33g of sodium chloride be excreted per day indefinitely?
No, 33g of sodium chloride will not be excreted per day indefinitely. As soon as a person starts to become sodium deficient (as a result of increased sodium excretion), the usual sodium retaining reflexes will be set in motion. They will be unable to raise aldosterone secretion, but they will lower GFR and alter the other factors that stimulate tubular sodium reabsorption to compensate at least partially for the decreased aldosterone-dependent sodium absorption.
How is osmolality regulated?
Changes in renal water handling. Osmolality needs to change 1-2% before ADH comes into play (ADH is the mediator).
How is ECF volume regulated?
Changes in renal sodium handling. ECF volume varies a lot thought the day. The mediators: renin-angiotensin, and sympathetic nervous systems.
Why does ECF osmolality need to stay constant?
Most parts of our body do not like changes in osmolality, especially brain cells. The symptoms are:
What is hyponatremia?
Decreased sodium levels.
What happens when there is a decrease in ECF volume?
Decreased ECF volume is compensated by an increase in renal reabsorption of sodium. When ECF volume increases, there is less reabsorption of sodium.
What inhibits sodium reabsorption?
1. ANP = atrial natriuretic peptide (28 amino acids).
2. Urodilatin - which is released by the kidney. It is almost identical to ANP (30 amino acids).
3. Dopamine - released by neurons in the proximal tubules.
Where is ANP released from and why?
It is released in the atria (heart) in response to increased filling pressure and increased atrial stretch.
How does ANP work?
It binds to receptors to increasecGMP. It decreases sodium reabsorption in the distal tubule and outer medullary collecting tubule by: -blocking ENac
-inhibits the release of aldosterone and renin.
-vasodilation of the afferent arteriole to increase GFR.
What are the sensors for ECF volume regulation?
1. Carotid sinus.
2. Aortic arch.
3. Renal afferent arteriole.
What are the efferent pathways for ECF volume regulation?
1. Renin-angiotensin-aldosterone axis.
2. Sympathetic nervous system.
What is the effector for ECF volume regulation?
Short term = heart, blood vessels.
Long term = kidney.
What is affected in ECF volume regulation?
Short term = blood pressure.
Long term = sodium excretion.
What are the sensors for osmoalilty regulation?
What are the efferent pathways for osmolality regulation?
What is the effector in osmolality regulation?
2. Brain: drinking behaviour.
What is affected in osmolality regulation?
1. Renal water excretion.
2. Water intake.
What happens when you eat a lot of sodium?
Osmolality changes first - sensed in osmoreceptors in the hypothalamus. This will increase ADH secretion. Water reabsorption occurs. Osmolality goes back to normal. However there is an increase in volume, this is detected in the stretch receptors. This will cause the excretion of water.