Mineralocorticoid (Aldosterone)

Mineralocorticoid

(Aldosterone) Mineralocorticoids are the strongest naturally mineralocorticoids

Relation b/w Aldosterone and ADH

- Aldosterone from adrenal gland --> increased Na+ --> plasma osmolarity sensed by osmoreceptors in hypothalamus: osmoreceptors will signal --> hypothalamus --> ADH to post. pit. --> ADH --> collecting duct --> H2O --> decreased Na+, decreased plasma osmolarity ALDOSTERONE is important for regulation of increased [Na+ in total body], where ADH regulates the plasma Na+ concentration

Mechanics of aldosterone action:

- Aldosterone stimulates active transport of Na++ through epithelial cell - Aldosterone, like other steroid hormones, induces synthesis of proteins and the proteins are involved in following functions: 1) Increased Na+ transport by opening the Na+ channels in distal convoluted tubule 2) Increased number of Na-K ATPase molecules 3) May alter the membrane phospholipid composition

Regulation of Aldosterone

- Renin-angiotensin system regulates the secretion of aldosterone - aldosterone isnt dependent on ACTH, but ACTH required for normal levels - the stimulatory controllers are sensed by juxtaglomerular cells in the kidney , which secrete an enzyme called renin. A) decrease in BV causes a decrease in renal perfusion, which increases renin secretion. B) Angiotensin II acts on zona glomerulosa cells to increase conversion of corticosterone to aldosterone C) Aldosterone --> increased Na --> increased volume of ECF --> blood volume

Hypocalcemia

- abnormally low level of calcium in the blood - prolonged ST and QT intervals

Hypercalcemia

- the presence of abnormally high levels of Ca in blood - short ST segment and wide T wave

Clinical symptoms

1) Hypertension (aldosterone increases Na+ reabsorption) 2) Hypokalemia (aldosterone increases K+ secretion) 3) Metabolic alkalosis (b/c aldosterone decreases H+ secretion) 4) General symptoms of fatigue and weakness, polyuria 5) Decreased renin secretion (b/c increased aldosterone)

Functions of aldosterone:

1) Renal Na+ retention (absorption) 2) Na+ intake low- increased renin secretion - increase in plasma angiotensin II, which stimulates aldosterone secretion - also, Na+ reabsorption in sweat glands, colon. - increased renal K+, NH4, and H4 secretion

Why cortisol does not bind to mineralocorticoid receptors in the kidneys and other locations and produce mineralocorticoid effects?

Kidneys and other aldosterone sensitive tissues contain the enzyme 11-B hydrosteroid dehydrogenase-2. This enzyme leaves aldosterone untouched, but it converts cortisol --> corticosterol --> II-oxy derivative (do not bind to receptors)

Conn's Syndrome

Primary aldosteronism, - aldosterone secreting adenoma, which is unilateral (75%) and 25% cases are bilateral adrenal hyperplasia

Transport of Aldosterone

Transport in blood, aldosterone binds with low affinity to plasma albumin, transcortin and specific aldosterone globulin.

Treatment for 1 and 2 aldosteronism

aldosterone antagonist (high doses)

Secondary Aldosteronism

any cause of low blood volume (hemorrhage, dehydration) leads to increased renin and aldosterone secretion

Primary Aldosteronism

caused by aldosterone secreting tumors

Hyperaldosteronism

clinical state that results from increased aldosterone

Hypokalemia

deficient level of potassium in the blood - ST depression - prominent U wave, shallow, flat inverted T wave

Hyperkalemia

excessive potassium in the blood - tall peaked T waves, flat P waves, wide QRS complex, and prolonged PRI interval

Atrial Natriuretic Peptide

A peptide hormone secreted by cardiac atrial cells in response to atrial distension (increased blood flow); causes increased renal sodium excretion and as such lowers blood pressure (antagonizing aldosterone). ANF inhibits aldosterone production