1.
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
2.
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)
3.
Conn's Syndrome: Primary aldosteronism, - aldosterone secreting adenoma, which is unilateral (75%) and 25% cases are bilateral adrenal hyperplasia
4.
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
5.
Hyperaldosteronism: clinical state that results from increased aldosterone
6.
Hypercalcemia: - the presence of abnormally high levels of Ca in blood
- short ST segment and wide T wave
7.
Hyperkalemia: excessive potassium in the blood
- tall peaked T waves, flat P waves, wide QRS complex, and prolonged PRI interval
8.
Hypocalcemia: - abnormally low level of calcium in the blood
- prolonged ST and QT intervals
9.
Hypokalemia: deficient level of potassium in the blood
- ST depression - prominent U wave, shallow, flat inverted T wave
10.
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
11.
Mineralocorticoid: (Aldosterone)
Mineralocorticoids are the strongest naturally mineralocorticoids
12.
Primary Aldosteronism: caused by aldosterone secreting tumors
13.
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
14.
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
15.
Secondary Aldosteronism: any cause of low blood volume (hemorrhage, dehydration) leads to increased renin and aldosterone secretion
16.
Transport of Aldosterone: Transport in blood, aldosterone binds with low affinity to plasma albumin, transcortin and specific aldosterone globulin.
17.
Treatment for 1 and 2 aldosteronism: aldosterone antagonist (high doses)
18.
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)
