Secondary hyperaldosteronism pathophysiology: Difference between revisions

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=== Renin-angiotensin system components ===
=== Renin-angiotensin system components ===
Renin: 
[[Renin]]
* In each kidney there is a specialized system called juxtaglomerular system, which is located in afferent arteriole of each glomerulus.
* In each [[kidney]] there is a specialized system called [[juxtaglomerular apparatus]], which is located in [[afferent arteriole]] of each [[glomerulus]].
* These apparatus synthesizes prorenin, and then later it converts into renin with mediation of a proteolytic enzyme.  
* [[Juxtaglomerular apparatus]] synthesizes prorenin, and then later it converts into [[renin]] with mediation of a [[proteolytic enzyme]].  
* Renin stores in and then may be released from secretory granules, in response to various factors.  
* [[Renin]] stores in and then may be released from secretory [[granules]], in response to various factors.  
* Renin releasing starts a cascade of steps, and the first step is the cleavage of the angiotensin I from  angiotensinogen (renin substrate).
* [[Renin]] releasing starts a cascade of steps, and the first step is the cleavage of the [[angiotensin]] I from  [[angiotensinogen]] ([[renin]] substrate).
* Angiotensinogen is an alpha-2-globulin that is produced in the liver and kidney and other organs.
* [[Angiotensinogen]] is an alpha-2-globulin that is produced in the [[liver]] and [[kidney]] and other organs.
* The first step is the rate-limiting step of the renin-angiotensin cascade.  
* The first step is the rate-limiting step of the [[Renin-angiotensin system|renin-angiotensin]] cascade.  
* Most important stimuli to renin secretion are :
* Most important stimuli to [[renin]] secretion are :
** Renal hypoperfusion, due to hypotension or volume depletion
** [[Renal]] hypoperfusion, due to hypotension or [[volume depletion]]
** Increased sympathetic activity.
** Increased [[sympathetic]] activity.


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[[Image:Renin-angiotensin system in man shadow.png|600px|center|Renin angiotensin system, by Mikael Häggström - https://commons.wikimedia.org/w/index.php?curid=8458370]]
[[Image:Renin-angiotensin system in man shadow.png|600px|center|thumb|Renin angiotensin system, by Mikael Häggström - https://commons.wikimedia.org/w/index.php?curid=8458370]]





Latest revision as of 21:38, 28 September 2017

Secondary hyperaldosteronism Microchapters

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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


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".