adrenocortical tissue (cortex)
glandular steroidogenic secretes:
- cortisol/corticosterone
- aldosterone
- androgens
medullary or chromaffin tissue
- stains w/ chromic dyes (characteristic of all sympathetic neurons)
- secretes E & NE
- E & NE controlled separately by hypothalamus via sympathetic nervous system
zona glomerulosa
- outermost region (smallest portion of cortex)
- secretes aldosterone (not controlled by ACTH)
- Renin-Angiotensin System =RAS
zona fasciculata
- largest region
- secretes cortisol (F) and/or corticosterone (B)
- controlled by ACTH
- hypophysectomy -> atrophy of z.f. (removal of pituitary)
- ACHT -> hypertrophy of z.f.
zona reticuarlis
-innermost region
-secretes:
AND, DHEA, DHEAS
-controlled by ACTH or LH
-secretion peaks at puberty = adrenarche
adrenarche
- androgen secretion coming from the adrenals
- occurs at puberty for both
the fetal zone
- largest zone at birth in human
- size of adult adrenal at birth
- shrinks rapidly after birth
- important for steroid (androgen) synthesis during pregnancy
glucocorticoid secretion
controlled by ACTH
diurnal/circadian rhythms
human: -ACTH peaks 6-9 am -cortisol peaks 7-9 am rat: -nocturanl -inverse pattern
adrenopause
- accelerates at puberty
- remains high until middle age
- declines begin b/w 40 & 50 yrs
actions of glucocorticoids: types of action
1) metabolism (include permissive)
2) immune
3) repro & devel
4) brain func
5) permissive
actions of glucocorticoids: effects on metabolism
1) inhibits glucose uptake by peripheral tissues
2) stimulates gluconeogenesis
inhibiting glucose uptake by peripheral tissues
- everything except CNS
- especially inhibits muscle uptake of glucose (except CNS)
- may induce temporary hyperglycemia
- -glucocorticoids make sure all the necessary tissues will give up their share of glucose
stimulating gluconeogenesis: activates enzyme PEPCK in liver
- phosphoenolpyruvate carboxykinase
- liver and kidneys only
stimulating gluconeogenesis: alters amino acid metabolism
- causes protein catabolism in muscle
- increases plasma AA levels
- stimulates AA uptake by liver
- ->more gluconeogenic substrate
- ->glucose->blood
stimulating gluconeogenesis: enhances lipolysis caused by other hormones
- ->increases NEFAs & glycerol in plasma
- ->more gluconeogenic substrate
- ->glucose
glucocorticoids alters immune function
- GCs can suppress inflammation
- GCs can enhance T-cells
glucocorticoids influence on reproduction & development
1) fetal development & pregnancy
2) inhibition of GTH secretion
glucocorticoids influence of brain function
affects hippocampus
- chronic high GCs impair acute memory
- chronic high GCs prevent neurogenesis
- chronic high GCs cause neurodegeneration
glucocorticoids permissive actions
- affect membrane permeabilities
- affect certain enzyme levels
- therefore, may affect actions of other regulators
e. g. insulin, glucagon, catecholamine, GH
pathological & pharmacological effects of GCs
-can induce mellitus (prolonged elevation of blood glucose)
-can influence salt balance (normally can’t influence MC targets)
F->cortisone
-cortisone does not bind to MR but chronic high levels of F can alter Na/K balance
if you administered metyrapone (blocks P450c11) what will happen to the adrenal cortex?
enlarge
functions of aldosterone
distal convoluted tubule
- stimulates Na/K exchange
- Na reabsorption
- K secretion
- H2O follows Na
regulation of aldosterone secretion
1) RAS
2) ACTH (modest & transient)
