Study sets, textbooks, questions
Upgrade to remove ads
Terms in this set (28)
where is aldostrone produced
physi effects and its control
where is it produced
produced by zona glomerulosa of adrenal cortex
It is the only zone that contains aldosterone synthase.
control of synthesis
ACTH also stimulates aldosterone synthesis.
In the absence of ACTH, sodium depletion still activates renin-angiotensin system to stimulate aldosterone synthesis.
Aldosterone levels — highest concentration being at 8 AM, lowest at 11 PM, in parallel to cortisol rhythms.
steps of production
Cholesterol converted to Pregnenolone
Aldosterone synthase is responsible for the last three steps
Conversion from 11-deoxycorticosterone to corticosterone is normally by 11beta-hydroxylase in other part of adrenal gland.
--> In zona glomerulosa, 11beta-hydroxylase is absent and conversion is done by aldosterone synthase
about 20 minutes
slightly bond to protein only
Most converted to tetrahydroglucuronide derivative in liver
Some converted to 18-glucuronide in liver and kidney
* Reverts back to free aldosterone at pH 1
* i.e. acid-labile conjugate
Less than 1% excreted in urine in free form.
MOA of aldosterone
Cross freely into principle cells
--> Combine with mineralocorticoid receptors in the cytoplasm
--> Receptor acts as transcription factor
--> synthesis of specific mRNA and protein
--> Increase activity/number of apical sodium channel and basolateral Na-K ATPase pump
increase serum glococorticoid regulated kinase, Increase in ENaC (epithelial sodium channel) is in 2 phases:
* Rapid effect by increasing insertion from cytoplasmic pool of ENaCs
* Slower effect by increasing synthesis of ENaCs
ENaC is inhibited by amiloride [WG21:p34]
The movement of Na+ through its channel ENaC is electrogenic, creates a lumen-negative potential difference.
Electroneutrality is maintained in this setting either by passive Cl- reabsorption via the paracellular pathway or by K+ secretion from the cell into the lumen
Action of aldosterone
* Sodium resorption
* Increase urinary K+ loss
* Increase urinary H+ loss
* facilitate K movement into cells along with adrenaline and insulin
Sodium is in effect reabsorbed in exchange for K+ and H+
--> Aldosterone increases urines K+ loss and urinary acidity
how control Na reabsoprtion
Mainly by the cortical connecting tubule and cortical collecting duct.
Sodium reabsorption is by principle cells
* Principle cells are also the site of water regulation by ADH
Stimulate sodium transport by other epithelia such as sweat, salivary duct, colonic mucosa
--> All promote sodium retention
Effect takes 10-30 minutes to develop and even longer to peak
how increase K loss in urine
stimulate K secretion in principal cells of cortical collecting duct and late DCT; control the final 2% of tubular Na reasborption; fine tuning of sodium excretion
how stimulate H secretion in urine
Some Na+ - H+ exchange at apical membrane of principal cell
Increase H+-ATPase activity
Overall[ INCREASE H+ secretion
Control of aldstrone secretion
3 main factors ACTH (transient effect only)
Increased in plasma [K+]
* Direct effect on adrenal cortex
Plasma Na conc, dopamine / ANP
Effect of Ag II on aldosterone
Angiotensin II binds to AT1 receptors in the zona glomerulosa
--> Act via G protein
--> Activating phospholipase C
--> In increased protein kinase C
Stimulates conversion of cholesterol to pregnenolone
Stimulates conversion of corticosterone to 18-hydroxycorticosterone
Only angiotensin II produces a change in aldosterone that is directly related to sodium balance
Effect of ACTH on aldosterone
Transient stimulatory effect on aldosterone
Aldosterone output declines after 1-2 days of elevated ACTH
stimulate on at high concentration eg surgery, trauma
Effect of K on aldosterone
Need to increase only by 1meq/L to stimulate aldosterone secretion
Acts by depolarising the cells
--> Opening up voltage-gated Ca2+ channels
--> Increase intracellular Ca2+
Increases sensitivity of zona glomerulosa to angiotensin II
so can increase K excretion
Plasma Na effect on aldosterone
increase aldostreon production when hyponatremia
Dopmine / ANP
inhibit aldosreone seceretion
Mineralocorticoid receptors actually have higher affinity for glucocorticoids than glucocorticoid receptors do
* i.e. glucocorticoids bind to mineralocorticoid receptor better than to glucocorticoid receptors
In kidney and other mineralocorticoid-sensitive tissues, enzyme (11beta-hydroxysteroid dehydrogenase type 2) is present that converts cortisol and corticosterone into steroid forms that do not bind to the mineralocorticoid receptors.
If this enzyme is absent or inhibited (e.g. by prolonged ingestion of licorice)
--> Cortisol has marked mineralocorticoid effect
--> Apparent mineralocorticoid excess syndrome
Aldosterone role in controlling K
Aldo Principle #校長@ CC college
aldosterone stimulate K secretion by principal cells of cortical collecting tube.
increase no of basolateral Na/K ATPase pump and open K channel in the luminal membrane, which facilitate K secretion into tubules
3 primary factors stimulating aldosterone release
- ACTH (transient effect only)
- Angiotensin II
- Increased in plasma [K+]
* Direct effect on adrenal cortex
why standing increase aldosterone
Aldosterone release is increased in standing position because
Decreased hepatic clearance
Increase in renin and hence angiotensin II
ANP'r role in aldosteron
ANP inhibits renin secretion and decrease responsiveness of the zona glomerulosa to angiotensin II
ANP inhibits aldosterone
Primary hyperaldosteronism cause what?
metabolic alkalosis with increase ECF, hypokalaemia and hypochloraemia.
caused by primary overproduction of aldosterone in conditions such as Conn's syndrome.
Don't get edema, because increase in intravascular volume, will trigger ANP, therefore only hypertension
Kaliuresis (K in urine)
increase ECF / increase BP
Conditions of low cardiac output are also known to stimulate synthesis of aldosterone.
cirrhosis - diminished breakdown of aldosterone
Both conditions result in sustained hypertension.
Sets found in the same folder
Describe the renal factor that affect ur…
buffer, phosphate, ammonia, acid base of kidney
Autoregulation of Renal
Infusion of 1N HCI
Sets with similar terms
18. Renal System (42) & (43)
Hormone and Metabolism control
ENDO Chapter 6 Multiple choice
Other sets by this creator
spanish vocab 15
Other Quizlet sets
Pharm chap 12
Domain 2: Nutrition Care (Topic A - Screening and…
Speaking questions - TOPIC A (second part town) +…
What hypothalamic hormone stimulates the release of ACTH
Why must you rotate sites of insulin injection?
why is it important to know the onset, peak and duration of insulin?
How does epinephrine regulate glycogen phosphorylase in the muscle?