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Aldosterone, secreted by the glomerulosa cells of the adrenal cortex, stimulates the active uptake of [[Sodium|sodium]] (Na+), and consequently [[Water|water]], from the glomerular filtrate in the distal tubules of the [[Kidney|kidney]]. Aldosterone synthesis and release is controlled by the [[Renin-Angiotensin System|renin-angiotensin system]]. <ref name="Nussey S, Whitehead S.(2001)">http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&amp;amp;amp;part=A442#A635</ref> | Aldosterone, secreted by the glomerulosa cells of the adrenal cortex, stimulates the active uptake of [[Sodium|sodium]] (Na+), and consequently [[Water|water]], from the glomerular filtrate in the distal tubules of the [[Kidney|kidney]]. Aldosterone synthesis and release is controlled by the [[Renin-Angiotensin System|renin-angiotensin system]]. <ref name="Nussey S, Whitehead S.(2001)">http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&amp;amp;amp;amp;part=A442#A635</ref> | ||
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=== <u>Mechanism of Action</u> === | === <u>Mechanism of Action</u> === | ||
In the circulation aldosterone (A) is mainly bound to [[ | In the circulation aldosterone (A) is mainly bound to [[Cortisol-binding globulin|cortisol-binding globulin ]](CBG) or albumin. | ||
*Free aldosterone enters the tubule cells of the kidney and binds to the [[ | *Free aldosterone enters the tubule cells of the kidney and binds to the [[Mineralocorticoid receptor|mineralocorticoid receptor ]](MR). | ||
*This induces release of a [[ | *This induces release of a [[Heat shock protein|heat shock protein ]](hsp), dimerization of two MRs and translocation to the nucleus. | ||
*Where it binds to a [[ | *Where it binds to a [[Glucocorticoid response element|glucocorticoid response element ]](GRE) on the [[DNA|DNA]] and, along with other transcription factors, initiates [[Protein|protein synthesis]] | ||
*The aldosterone-induced proteins include factors that regulate the luminal Na+ channel and components of the [[Na+/K+ ATPase pump|Na+/K+ ATPase pump]]. | *The aldosterone-induced proteins include factors that regulate the luminal Na+ channel and components of the [[Na+/K+ ATPase pump|Na+/K+ ATPase pump]]. | ||
<u></u> <ref name="Nussey S, Whitehead S. (2001)">http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&part=A442&rendertype=box&id=A647</ref> | <u></u> <ref name="Nussey S, Whitehead S. (2001)">http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin&amp;part=A442&amp;rendertype=box&amp;id=A647</ref> | ||
=== <u>Health and Diease</u> === | === <u>Health and Diease</u> === | ||
Imbalances in aldosterone can cause numerous health problems e.g. excessive aldosterone synthesis(hyperaldosteronism) and release may lead to [[Hypertension|hypertension]]. [[Hypertension|Hypertension]] is a risk factor in the development of diseases of the heart, vasculature and other organs such as the kidneys. Continued high blood pressure is cited as the commonest cause of stroke, which results from either blockage or, less commonly, haemorrhage of vulnerable blood vessels in the brain. | |||
[[Hyperaldosteronism|Hyperaldosteronism]] is the most likely common cause of mineralocorticoid hypertension and may occur in 0.01% to 0.03% of patients. Symptoms include sodium retention, heart rhythm irregularities and possibly muscle weakness as well as spontaneous or diuretic-induced [[hypokalaemia|hypokalaemia]]. <ref name="National Institute for Health and Clinicial Excellence(2009)">http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=nicecg18&part=evidence#evidence.s39</ref><br> | |||
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=== <u>References</u> === | === <u>References</u> === | ||
<references /> | <references /> | ||
Revision as of 14:42, 18 November 2010
Aldosterone, secreted by the glomerulosa cells of the adrenal cortex, stimulates the active uptake of sodium (Na+), and consequently water, from the glomerular filtrate in the distal tubules of the kidney. Aldosterone synthesis and release is controlled by the renin-angiotensin system. [1]
Mechanism of Action
In the circulation aldosterone (A) is mainly bound to cortisol-binding globulin (CBG) or albumin.
- Free aldosterone enters the tubule cells of the kidney and binds to the mineralocorticoid receptor (MR).
- This induces release of a heat shock protein (hsp), dimerization of two MRs and translocation to the nucleus.
- Where it binds to a glucocorticoid response element (GRE) on the DNA and, along with other transcription factors, initiates protein synthesis
- The aldosterone-induced proteins include factors that regulate the luminal Na+ channel and components of the Na+/K+ ATPase pump.
Health and Diease
Imbalances in aldosterone can cause numerous health problems e.g. excessive aldosterone synthesis(hyperaldosteronism) and release may lead to hypertension. Hypertension is a risk factor in the development of diseases of the heart, vasculature and other organs such as the kidneys. Continued high blood pressure is cited as the commonest cause of stroke, which results from either blockage or, less commonly, haemorrhage of vulnerable blood vessels in the brain.
Hyperaldosteronism is the most likely common cause of mineralocorticoid hypertension and may occur in 0.01% to 0.03% of patients. Symptoms include sodium retention, heart rhythm irregularities and possibly muscle weakness as well as spontaneous or diuretic-induced hypokalaemia. [3]