Aldosterone Deanna Page.

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Presentation transcript:

Aldosterone Deanna Page

SYNTHESIS Aldosterone is synthesized by the cells of the Zona Glomerulosa of the Adrenal Cortex in the Adrenal Gland, located above the Kidneys.

STRUCTURE C21H28O5 A steroid hormone, class of corticosteroids (steroid produced in the adrenal cortex), main mineralocorticoid (class of corticosteroid, produced in the adrenal cortex)

REGUALTION AND ACTION Synthesis of aldosterone is stimulated by elevated levels of blood potassium Angiotensin II, a product of the renin-angiotensin-aldosterone system. Directly stimulates the reabsorption of sodium and the excretion of potassium by principal cells of the distal tubule and the collecting duct.  indirectly influences blood pressure, blood volume, and water retention.

Renin Angiotensin Aldosterone Pathway

Create Na+/K+ pump to drive K+ ions into the principal cell of collective duct. Creates K+ channels on the apical surface of the principal cell to allow K+ to flow through passive transport to the urine Creates Na+ channels on the apical surface of the principal cell to allow Na+ from the urine into the principal cell, then through the Na+/K+ pump into the blood. High concentration of Na+ in blood causes osmosis to occur, so water from the urine will come into the blood Increased stroke volume = Increased blood pressure

Goal: Bring in Na+ from urine into the bloodstream through different channels

How do leftover protons escape cell? Proton pump Sodium proton pump Potassium proton pump H+ H+ H2O + CO2 → H2CO3 ⇒ H+ + HCO3- Na+ Stimulates secretion of H+, rremoves excess protons from blood H+ K+ Goal: Get rid of leftover protons in alpha intercalated cell through pumps that also power the aldosterone pathway to increase blood pressure

Juxtaglomerular (JG) cells = primary site of renin storage and release reduction in afferent arteriole pressure  release of renin from the JG cells increased pressure  inhibits renin release. Specialized cells (macula densa) = senses the concentration of sodium and chloride ions in the tubular fluid NaCl is elevated in the tubular fluid  inhibits renin release reduction in tubular NaCl  stimulates renin release by the JG cells

MINERALCORTICOID RECEPTOR ALDOSTERONE RECEPTOR It belongs to the nuclear receptor family where the ligand diffuses into cells, interacts with the receptor and results in a signal transduction affecting specific gene expression in the nucleus.

LOW LEVELS VS HIGH LEVELS Low Levels of Aldosterone: --dehydration, low blood pressure, a low blood sodium level, and a high potassium level, high pulse --symptoms of fatigue and often salt-craving, “cognitive fuzziness”, dizziness or lightheadedness on standing, or palpitations High Levels of Aldosterone: --increases reabsorption of sodium and loss of potassium by the kidneys, low potassium level, high blood pressure --symptoms include headache and muscle weakness, especially if potassium levels are very low

THE END