Secondary hyperaldosteronism pathophysiology

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Overview

Secondary hyperaldosteronism is a disease of increasing aldosterone or other mineralocorticoid levels. The resulting Na+ retention produces hypertension, and elevated K+ excretion may cause hypokalemia.

Pathophysiology

Renin-angiotensin system components

Renin

Renin-angiotensin system components Secretion control Measurement Inhibition
Renin 
  • Baroreceptors (or stretch receptors) in the wall of the afferent arteriole
  • Cardiac and arterial baroreceptors, which regulate sympathetic neural activity and the level of circulating catecholamines, both of which enhance renin secretion via the beta-1-adrenergic receptors
  • The cells of the macula densa in the early distal tubule, which appear to be stimulated by a reduction in chloride delivery, particularly in the chloride concentration in the fluid delivered to this site
  • The plasma renin activity (PRA) is an indirect measure of renin that employs an enzyme-kinetic bioassay, which measures its capacity to generate angiotensin I. The rate of angiotensin I production, and therefore PRA, is critically dependent upon the concentration of substrate in plasma (ie, angiotensinogen).
  • The plasma renin concentration (PRC) employs a direct immunosorbent assay that detects both prorenin and renin
Angiotensinogen 
Angiotensin-converting enzyme 
Angiotensin II
Aldosterone 

Basic physiology of aldosterone

Circulating aldosterone is principally made in the zona glomerulosa of the adrenal cortex (outer layer of the cortex) by a cascade of enzyme steps leading to the conversion of cholesterol to aldosterone.  


Renin angiotensin system, by Mikael Häggström - https://commons.wikimedia.org/w/index.php?curid=8458370
Renin angiotensin system, by Mikael Häggström - https://commons.wikimedia.org/w/index.php?curid=8458370


Adrenal steroid synthesis pathways in adrenal cortex and related enzymes [2]

Pathogenesis

Secondary hyperaldosteronism syndrome is a disease of increasing aldosterone or other mineralocorticoid levels. The resulting Na+ retention produces hypertension, and elevated K+ excretion may cause hypokalemia. Patients with Secondary hyperaldosertonism may have:

Genetics

References

  1. Williams GH (2005). "Aldosterone biosynthesis, regulation, and classical mechanism of action". Heart Fail Rev. 10 (1): 7–13. doi:10.1007/s10741-005-2343-3. PMID 15947886.
  2. "File:Adrenal Steroids Pathways.svg - Wikimedia Commons".