Renin–Angiotensin–Aldosterone System Flashcards
Renin–Angiotensin–Aldosterone System
Decreases in blood volume cause a decrease in renal perfusion pressure, which in turn increases renin secretion. Renin, an enzyme, catalyzes the conversion of angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE).
Renin–Angiotensin–Aldosterone System
Angiotensin II acts on the zona glomerulosa of the adrenal cortex to increase the conversion of corticosterone to aldosterone.
Renin–Angiotensin–Aldosterone System
Aldosterone increases renal Na+ reabsorption, thereby restoring extracellular fluid (ECF) volume and blood volume to normal.
Renin–Angiotensin–Aldosterone System
Hyperkalemia increases aldosterone secretion. Aldosterone increases renal K+ secretion, restoring blood [K+] to normal.
Actions of mineralocorticoids (aldosterone)
↑ renal Na+ reabsorption (action on the principal cells of the late distal tubule and collecting duct)
Actions of mineralocorticoids (aldosterone)
↑ renal K+ secretion (action on the principal cells of the late distal tubule and collecting duct)
Actions of mineralocorticoids (aldosterone)
↑ renal H+ secretion (action on the α-intercalated cells of the late distal tubule and collecting duct)
Hyperaldosteronism—Conn’s syndrome
is caused by an aldosterone-secreting tumor.
Hyperaldosteronism—Conn’s syndrome
Hypertension (because aldosterone increases Na+ reabsorption, which leads to increases in ECF volume and blood volume)
Hyperaldosteronism—Conn’s syndrome
Hypokalemia (because aldosterone increases K+ secretion)
Hyperaldosteronism—Conn’s syndrome
Metabolic alkalosis (because aldosterone increases H+ secretion)
Hyperaldosteronism—Conn’s syndrome
decreased renin secretion (because increased ECF volume and blood pressure inhibit renin secretion by negative feedback)
Hypoaldosternism
The lack of aldosterone has three direct effects on the kidney: decreased Na+ reabsorption, decreased K+ secretion, and decreased H+ secretion. As a result, there is ECF volume contraction (caused by decreased Na+ reabsorption), hyperkalemia (caused by decreased K+ secretion), and metabolic acidosis (caused by decreased H+ secretion).
Hypoaldosternism
The ECF volume contraction is responsible for orthostatic hypotension. The decreased arterial pressure produces an increased pulse rate via the baroreceptor mechanism.
Hypoaldosternism
ECF volume contraction also stimulates ADH secretion from the posterior pituitary via volume receptors. ADH causes increased water reabsorption from the collecting ducts, which results in decreased serum [Na+] (hyponatremia) and decreased serum osmolarity.
