Hormone: Mineral Corticoid (Zona glomerulosa)

Basic: Steroid, Non-tropic, hormonal

Location: Adrenal Cortex (zone glomerulosa)
Mechanism: Hormonal control
Stimulated by:

Direct:
Decreasing Na+ in the blood
Increased K+ in the blood
Decreasing blood volume and blood pressure
Indirect:
Renin-angiotensin mechanism
ACTH and CRH only have minor effects on aldosterone release

Negative feedback mechanism:

Increasing Na+ blood levels, decreasing K+ blood levels, increasing blood volume, blood
pressure, increasing ANF (Atrial natriuretic factor) will inhibit aldosterone release from zona
glomerulosa

Target:

Kidney:
Stimulates Na+ reabsorption and water retention by elimination of K+
Brings Na+ back into the blood thus increasing BV and BP

Action:

Increases Na+ blood levels

Decreased K+ blood levels
Increased BV and BP

Disease:

Hyperaldosteronism:
S/S:
o Decreased K+ -> hypopolarization-> alteration of electrical excitability of
neurons and muscle cells causing -> muscle weakness develops

Hypoaldosteronism:
S/S:
o Decreased Na+ and H2O reabsorption-> decreased BV-> BP

Increased K+ (by 60 to 100%) -> serious heart toxicity, weakness of heart

contraction, and the development of arrhythmia-> can lead to heart failure

Addisons Disease:
Lack of all categories of specific hormones from adrenal cortex. Usually due to the
destruction of entire adrenal cortex. Majority of cases are caused by autoimmune
destruction
Effects:
o Lack of Aldosterone:
Inability to reabsorb Na+ and water from kidneys; not enough water is
reabsorbed via ADH and a low blood volume causes hypotension,
particularly with changes in pressure
Hyperkalemia (low K+ blood levels)
Renin-Angiotensin II mechanism is activated-> Incr. rennin (in response
to low glomerular filtration rate-GFR
Any condition that results in low GFR will activate rennin cascade
o Lack of Androgens (Testosterone)
Female: decrease in body hair, especially in pubic and axillary regions,
and hair on extremities
Male: No effect due to high level of testosterone production by testes
o Lack of cortisol:
Inability to mobilize amino acids
Decrease in gluconeogenesis
An overall inability to resit any type of biological stress such as infection
No cortisol in blood to feedback hypothalamus, hypothalamus
continues to direct anterior pituitary to release ACTH to stimulate
adrenal cortex. An over-production of ACTH mimic MSH due to similar
amino acid sequencing, especially on sunlight exposed skin