Primary aldosteronism

Endocrine hypertension accounts for approximately 10-15 % of all hypertension cases. The most frequent causes of endocrine hypertension are primary aldosteronism, Cushing's syndrome and pheochromocytoma. Other causes include hyperthyroidism, primary hyperparathyroidism and acromegaly.  

Primary aldosteronism (or Conn's syndrome) is characterised by an increased aldosterone concentration and by suppression of renin levels. The hormone aldosterone is produced from cholesterol in the adrenal cortex. It is a mineralocorticoid and is mainly regulated via the renin-angiotensin-aldosterone system (RAAS). 

Low blood pressure triggers the RAAS by stimulating the secretion of the protease renin from the juxtaglomerular cells of the kidney into the blood. Renin cleaves the glycoprotein angiotensinogen to form angiotensin I (Ang I). Ang I is processed into Ang II by the activity of the angiotensin-converting enzyme (ACE). Ang II, in turn, stimulates the production of the hormone aldosterone. 

Aldosterone acts mainly in the kidneys, increasing the resorption of sodium and water from the distal tubules into the blood and the excretion of potassium. This ultimately results in an increase of blood volume and blood pressure. 

In addition to the RAAS, Aldosterone secretion is also regulated by electrolyte concentrations, with potassium stimulating hormone release and sodium inhibiting it. 

In primary aldosteronism the excess secretion of aldosterone is intrinsic to the adrenal glands, irrespective of the levels of Ang II stimulation and electrolyte concentrations. This is most commonly due to an aldosterone producing adenoma or to bilateral adrenal hyperplasia. As an effect of the resulting high blood pressure, renin levels are suppressed.