Aldosterone and Adrenal Medulla Flashcards
Layers of the adrenal gland & what they release
Glomerulosa: releases aldsterone: in response to AGII from RAAS system
(some trigger by acth but mainly RAAS)
aldosterone is made here: and no other choleserol-related hormones are because there is NO 17-alpha hydroxylase present; therefore there cna be no conversion to teh cholesterol based hormones
Fasiculata: cortisol secretion & androgens : triggered by ACTH
Reticularis: cortisol and androgens: triggered by ACTH
medulla (inner most): SNS stimulation to secrete epinehrine and norepi.
When is aldosterone released from the adrenal cortex
- what are the triggers
- what does aldosterone do
- how much is in the plasma
- a decreased GFR (like renovascualr disease) : a trigger in attempts to increase volume flow
- increased sympathetic activity which decreased renal volume flow: will attemp to increase volume
- a decrease in sodium or cholride reaching the macula densa: triggers aldosterone
- direct elevation of potassium: triggers aldosterone
- hemorrhage or upright (hypovolemia)
aldosteron works to increase sodium reabsorbtion and increase potassium secretion in the distal CT and in collecting duct
How much in plasma
- aldosterone is not stored: equal amounts free and bound to albumin
- made as it is needed
so aldosterone will bind to mineralocorticoid receptors when..
- sodium is low
- potassium is high
- fluid volume low
by
- increasing sodium/potassium pumps, opening sodium channels and using cotransporters of sodium, chloride and potassium
Explain the receptors (mineralocorticoid receptors) and the significance
exaclt what receptors does aldosteron act on in the kidney
these receptors can bind to both cortisol and aldosterone (hence why you get edema with steroid use)
- cortisol is much more prominent in the blood: so the action of cortisol removal by (11-hydroxysteroiddehydrogenase) is essential
In the Kidney: aldosterone targets Enac (epithelial sodium channels) which inititate a foration of preotines to open up more channels
- this increases the number of ATP/NA/K+ channels at the surface to pump Na+ in and K+ out
main regulators of aldosterone release
AG II (from RAAS), extracellular K+ & ACTH
- AGII: from the RAAS system which was triggered by low pressures
- extracellular K+ : depolarizes the membrane and increases calcium - triggers aldosterone
Hyperaldosteronism
primary aldosteronism
Hyperaldosteronism
- a classic form = hypokalemia (rare)
- a milder form = no hypokalemia BUT hypertension (because increased salt uptake aka increase fluid uptake)
Primary Hyperaldosteronism
- a common cause of resistant hypertension
- excessive aldosterone production due to either
- 1. a single adrenal adenoma (conns syndreom)
- 2. bilateral cortical hyperplasia
- 3. other minor forms due to adenomas and carcinomas
Symptoms
- frontal headaches
- muscular weakness, can lead to paralysis (because lacking K+)
- nocturia with polydipisa and polyuria (because Na+ retention)
- HTN, hypokalmiea, metabolic alkalosis
Hypertension
- common cause of resistant hypertension (200/100)
Hypokalemia
slow fixed pulse (due to hypokalemis)
Alkalosis
- the loss of potassium (K+) leads to a loss of intracellular cations (+) : therefore H+ moves into the cells to compensate and thus, alkalosis
Secondary aldosteronism
causes (renin and estrogen)
Renin
- a varient of renovascualr disease
- excess renin production at the kideys; leads to excessive aldosterone
- think of this with renal artery stenosis
lack fo blood flow to the kidneys - thinks volume depleted, increases aldosterone via increasing renin
Estrogen
- contraceptives
- elevates renin
- same patho as above: increased aldosterone
secondary aldosteronsim can be a casue of hypertension as well!
Adrenal Medulla
what is it
where
associaetd with
what do the chromaffin cells secrete here
the innermost layer of the adrenal gland: not related to teh actions of th ecortex
- reponsive to sympatheic stimuli
- made of chromaffin cells : pheochromocytes from the neural crest formation = aka just like postganglionic neurons (SNS)
Secretion from the Medulla
- chromaffin cells secrete catecholamines: epinephrine (only location this is secreted!) and norepinephrine
- stimulated by Ach preganglionic nerves in the splanchnic nerves
- NOT involved in endocrine feedback
how is epinephrine synthesized
phenylethynolamine N methyl transferase faciliates the conversion of norepinephrine to epinephrine in the chromaffin cells
Briefly
- Tyrosine converted to Dopa
- Dopa to dopamine
- brought to chromaffin cells (or sympatheic neurons)
- dopamine converted to norepinephrine
- transported to cytosol of chormaffin cells (if there)
- norepinephrine converted to epinephirne
- the conversion of enorepi to epi via PhenNmethyl trasnferase is only happening in the medulla becuase this is the only place this enzyme is present!!
then its trasnported back into teh granules of the cells until quickly released when needed for SNS stimulation
what does epinephrine do in the SNS
when is it stimualted
“fight or flight”
stimulated increase in
- cardaic output
- vasodilation of skeletal muslce
- vasoconstriction of skin and internal organs
- mental alterness
- smooth muscle relaxtion (gi, bladder,etc.)
- stimulared lipolysis, glycogenolysis
- glucagon secretion
decreased insulin secretion (no time to store!)
When
- times of hypoglycemia
- direct innervation signals to the meduall thorugh SNS
- anything stressful
response occurs within seconds
effects of the epinephrine is determiend by recepotr (alpha, beta) and by location/target organ
Pheochromocytoma
- rare, single tumor of the adrenal medulla
- characterized byb hypertension and paroxysms and attacks of HTN that come and go
-most of tehse adrenal tumors secrete norepi and epi
Symptoms
- sense of impending doom
- hyperglycemia (intermittent)
- symotoms taht mimic hyerthyroidsm
- postural fall in BP: due to issues with baroreflex, chrnic alpha-adrenergic induce constriction and volume depetion
