The document discusses the adrenal glands and their hormones. It focuses on aldosterone, which is secreted by the zona glomerulosa of the adrenal cortex. Aldosterone increases sodium reabsorption and decreases potassium reabsorption in the kidneys. Though aldosterone initially causes sodium retention and hypertension, the phenomenon of "aldosterone escape" causes urinary sodium to return to normal levels. The mechanism and regulation of aldosterone secretion and action are also described, as well as the condition of primary aldosteronism or Conn's syndrome which results from excess aldosterone secretion.

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2. Introduction
Adrenal glands:
• 2 in number
• Mass= 4g
• 2 Major segments:
1)Cortex (80% of total weight)
 Zona Glomerulusa: Secretes
 Aldosterone
 Zona Fasiculata: Secretes
 Cortisol
 Corticosterone
 Adrenal androgens/oestrogens (small
amounts)
 Zona Reticularis: Secretes
 Dehydroxyepiandrosterone (DHEA)
 Androstenedione
 Some glucocorticoids and oestrogens
2) Medulla (20% of total weight)
 Secretes adrenaline and noradrenaline

4. Synthesis of Adrenal Hormones
 Only cells of the Zona Glomerulusa can
produce Aldosterone as they contain
the enzyme Aldosterone Synthase
 Adrenocortical hormones are bound to
plasma proteins
 Cortisol:
 (90-95)% bound to Transcortin.
 (5-10)% is in free form.
 This allows Cortisol to degenerate slowly
with a half-life of (60-90) minutes.
 Aldosterone:
 60% is bound to plasma proteins
 40% is in free form
 This prevents Aldosterone to degenerate
slowly with a half-life of about 20 minutes
 Adrenal Hormones are metabolised in
the Liver
 75% excreted in urine; 25% excreted in
feaces

6. Mineralcorticoids
• Aldostrerone
• Deoxycorticosterone
• Corticosterone
• 9α- fludrocortisol
• Cortisol
• Cortisone
Functions:
Aldosterone acts upon principal cells of Collecting
Tubules and to a lesser extent in Distal Tubules &
Collecting duct to:
 Increase Renal Tubular reabsorption of Na+
 Decrease Renal Tubular reabsorption of K+
Excess Aldosterone Increases Tubular H+
secretion causing alkalosis
Excess Aldosterone Increases ECF and thus,
Arterial Pressure but has a small effect on Plasma
Concentration due to Aldosterone Escape

8. Aldosterone Escape
Aldosterone escape is a physiologic phenomenon that
occurs with hyperaldosteronism. Aldosterone initially
decreases urinary sodium increasing sodium retension
contributing to hypertension. This does NOT result in edema
because the sodium retention is short lived. Urinary sodium
returns to normal through a process called aldosterone
escape. There are 2 processes that account for this:
– Pressure natriuresis and diuresis. Increased blood
pressure decreases distal sodium resorption. Increased
blood pressure is transmitted to the peritubular
capillaries, so the resorption of solutes must overcome
an elevated hydrostatic pressure gradient. In the face of
this increased gradient, sodium resorption falls.
– Decreased proximal sodium resorption. Blood volume
expansion decreases proximal sodium reabsorption and
increases sodium delivery to the distal nephron and
overwhelms the aldosterone induced sodium
resorption.
Aldosterone escape also explains the delay in hypokalemia
found with primary hyperaldosteronism. The increased
potassium excretion occurs with aldosterone escape when the
increased sodium delivery (decreased proximal absorption,
i.e. escape) occurs with the increased aldosterone levels

9. Mechanism of Aldosterone Action
• Takes 30 minutes to produce new
mRNA in the cells
• 45minutes(another 15 minutes
before the rate of Renal Tubular
reabsorption of Na+ increases
• Takes several hours to reach MAX
effect
• Possible non-genomic actions of
Aldosterone:
– By binding to Cell-Membrane
receptors
– Takes <2minutes

10. Regulation of Aldosterone
• Regulation of Aldosterone
secretion is independent of
regulation of Cortisol &
Androgens in other layers.
Factors increasing Aldosterone
secretion:
1. Increased K+
2. Increased Angiotensin-2
3. Decreased Na+
4. ACTH (very small role) but
total absence decreases
Aldosterone (Permissive
Role)

11. Primary Aldosteronism
• Excess Aldosterone secretion caused due to
a defect in the Adrenal Glands
Conn’s Syndrome:
 Excess Aldosterone secretion due to a small
tumour in Zona Glomerulusa
Effects:
 Hypokalemia
 Metabolic Alkalosis
 Slight increase in ECF and blood volume
 Modest increase in Plasma not
concentration <(4-6)mEq/L
 Hypertension
 Occasional periods of muscle Paralysis due
to Decreased K+
 Decreased Renin concentration due to high
Negative Feedback from increased
Aldosterone.