Glucocorticoid remediable aldosteronism

Glucocorticoid remediable aldosteronism also describable as aldosterone synthase hyperactivity, is an

It is a cause of

Patients with GRA may be asymptomatic, but the following symptoms can be present:^{[citation needed]}

• Fatigue
• Headache
• High blood pressure
• Hypokalemia
• Intermittent or temporary paralysis
• Muscle spasms
• Muscle weakness
• Numbness
• Polyuria
• Polydipsia
• Tingling
• Hypernatraemia
• Metabolic alkalosis

Normal Physiology

Aldosterone synthesis

is stimulated by several factors:

by increase in the plasma concentration of

angiotensin III

.

by increased plasma

ACTH, or potassium

levels.

The ACTH stimulation test is sometimes used to stimulate the production of aldosterone along with cortisol to determine if primary or secondary adrenal insufficiency is present.

by plasma acidosis.

by the

stretch receptors located in the atria of the heart

.

by

pineal

extracts. It selectively stimulates secretion of aldosterone.

The secretion of aldosterone has a

diurnal rhythm

.

Control of aldosterone release from the adrenal cortex:

• The role of the renin–angiotensin system:

Angiotensin is involved in regulating aldosterone and is the core regulator. Angiotensin II acts synergistically with potassium.

• The role of
  nerves
  :

Aldosterone production is also affected to one extent or another by

posture, and probably emotion (anxiety, fear, and hostility)(including surgical stress

).

• The role of
  baroreceptors
  :

Pressure in the carotid artery decreases aldosterone

• The role of the juxtaglomerular apparatus
• The plasma concentration of potassium:

The amount of aldosterone secreted is a direct function of the serum potassium as probably determined by sensors in the carotid artery.

• The plasma concentration of sodium:

Aldosterone is a function of the inverse of the sodium intake as sensed via osmotic pressure.

• Miscellaneous regulation:

pituitary peptide, also has some stimulating effect on aldosterone probably by stimulating deoxycorticosterone formation which is a precursor of aldosterone

.

Aldosterone is increased by

physical exertion, endotoxin shock, and burns

.

Aldosterone feedback:

Feedback by aldosterone concentration itself is of a non-morphological character (that is, other than changes in cell number or structure) and is relatively poor so that electrolyte feedback predominates in the short term.^{[citation needed]}

Pathophysiology

The

The product of this hybrid gene is aldosterone synthase that is ACTH-sensitive^[2] in the zona fasciculata of the adrenal gland.^[3]

Although in normal subjects, ACTH accelerates the

Genetic testing is done to ascertain that the individual in question does indeed have the condition^[5]

Treatment

In GRA, the hypersecretion of aldosterone and the accompanying

See also

• Inborn errors of steroid metabolism
• Hyperaldosteronism
• Pseudohyperaldosteronism
• Apparent mineralocorticoid excess syndrome
• Aldosterone and aldosterone synthase

References