Mineralocorticoids
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Transcript of Mineralocorticoids
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Dr. Eman El Eter
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Small, triangular glands loosely attached to the kidneys
Divided into two morphologically and distinct regions:
- Adrenal medulla- Adrenal cortex
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Cortex: (Secretes steroid hormones)◦Glucocorticoids. ◦Mineralocorticoids.◦Androgens.
Medulla (Amino acid secretions)◦Catecholamines
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MineralocorticoidsAldosterone
• A steroid hormone, secreted by Zona glomerulosa Essential for life.Aldosterone exerts the 90% of the mineralocorticoid activityCortisol also have mineralocorticoid activity, but only 1/400th that of aldosterone. • Responsible for regulating Na+ reabsorption in the distal tubule and the cortical collecting duct.• Target cells are called “principal (P) cell”.
* Metabolized in the liver to tetrahydroglucuroind derivative.
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Maintains extracellular fluid volume by conserving body sodium. Aldosterone stimulates sodium & potassium transport in sweat glands, salivary glands, & intestinal epithelial cells.
(+) synthesis of Na-K-ATPase in target cells.
Stimulates the active secretion of potassium from the tubular cell into the urine.
Stimulates secretion of H+ by the kidney
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Regulation of Aldosterone Release
Serum K+
Angiotensin II
ACTH
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ACTH also stimulates aldosterone synthesis. However the ACTH stimulation is more
transient than the other stimuli and is diminished within several days.
ACTH provides a tonic control of aldosterone synthesis.
Aldosterone levels fluctuate diurnally—
highest concentration being at 8 AM, lowest at 11 PM, in parallel to cortisol rhythms.
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JGAA specialized collection of two cell types: Macula densa cells Juxtaglomerular cellslocated at the juncture of the afferent and efferent arterioles with a portion of the distal convoluted tubule of the nephron of the kidney
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Macula densa cells –◦ Specialized chemoreceptor cells in the wall of
the distal convoluted tubule ◦ respond to changes in solute concentration
(especially sodium levels) in the urine ◦ sensory information is conveyed to the
juxtaglomerular cells which will adjust their output of renin accordingly.
juxtaglomerular cells◦ Specialized smooth muscle cells which act as
mechanoreceptors which stretch in response to increases in the blood pressure of the afferent arteriole
◦ synthesize and secrete the enzyme renin
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Angiotensin II acts on the zona glomerulosa to stimulate aldosterone synthesis.
Angiotensin II acts via increased intracellular cAMP to stimulate aldosterone synthesis.
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Pathway of RAAS
Principal factor controlling Ang II levels is renin release.
Decreased circulating volume stimulates renin release via:- low BP (effects on JGA).- low [NaCl] at macula
densa (“NaCl sensor”)- Low renal perfusion
pressure (“renal” baroreceptor)
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Adrenal Cortex Dysfunctions
Hypoadrenalism – Addison’s Disease
• Adrenal cortex produces inadequate amounts of hormonesCauses: -autoimmunity against cortices 80% -tuberculosis, drugs, cancer/ irradiation
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Lack of aldosterone:◦ Increased sodium, chloride, water loss◦ Decrease ECF volume◦ Hyperkalemia◦ Mild acidosis◦ Increase RBC concentration◦ Plasma sodium decreases and may lead to
circulatory collapse. Decrease cardiac output – shock - death within 4 days to a 2 weeks if not treated.
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Hyperaldosteronism can be caused by:
Primary overproduction of aldosterone in conditions such as Conn’s syndrome.
Conditions of low cardiac output are also known to stimulate synthesis of aldosterone.
Both conditions result in sustained hypertension.
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Hypertension. Hypokalemia Nocturnal polyuria & polydipsia Increased tubular (intercalated cells)
hydrogen ion secretion, with resultant mild alkalosis.
Neuromuscular manifestations◦ weakness, paresthesia◦ intermittent paralysis
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Plasma supine aldosterone at 0800h > 15 ng/dl
Urinary aldosterone metabolites◦ 18-Monoglucuronide > 20
ug/24h
◦ Tetrahydroaldosterone > 65
ug/24h NaCl infusion/ suppression test -- > 10
ng/dl