by adrenoglomerulotropin, a lipid factor, obtained from 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 sympathetic nerves:Aldosterone production is also affected to one extent or another by nervous control which integrates the inverse of carotid artery pressure, pain, posture, and probably emotion (anxiety, fear, and hostility)(including surgical stress).The role of baroreceptors:Pressure in the carotid artery decreases aldosteroneThe 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:ACTH, a pituitary peptide, also has some stimulating effect on aldosterone probably by stimulating deoxycorticosterone formation which is a precursor of aldosterone. Aldosterone is increased by blood loss, pregnancy, and possibly by other circumstances such as 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. Pathophysiology
The genes encoding aldosterone synthase and 11β-hydroxylase are 95% identical and are close together on chromosome 8.
In individuals with GRA, there is unequal crossing over so that the 5 regulatory region of the 11-hydroxylase gene is fused to the coding region of the aldosterone synthase.The product of this hybrid gene is aldosterone synthase that is ACTH-sensitive in the zona fasciculata of the adrenal gland.Although in normal subjects, ACTH accelerates the first step of aldosterone synthesis, ACTH normally has no effect on the activity of aldosterone synthase. However, in subjects with glucocorticoid-remediable aldosteronism, ACTH increases the activity of existing aldosterone synthase, resulting in an abnormally high rate of aldosterone synthesis and hyperaldosteronism. Diagnosis
Genetic testing is done to ascertain that the individual in question does indeed have the condition

Treatment
In GRA, the hypersecretion of aldosterone and the accompanying hypertension are remedied when ACTH secretion is suppressed by administering glucocorticoids.Dexamethasone, spironolactone and eplerenone have been used in treatment. See also
Inborn errors of steroid metabolism
Hyperaldosteronism
Pseudohyperaldosteronism
Apparent mineralocorticoid excess syndrome
Aldosterone and aldosterone synthase

References


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