Na, K, and RAAS Flashcards
How is NaCl plasma concentration monitored?
There are not receptors that monitor NaCl concentrations in the plasma. However, changes in NaCl concentration affect blood volume, for which there are receptors.
High pressure Baroreceptors (volume receptors) are present in the heart, and the afferent arterioles of the kidney (JMA). they will identify low pressure and act to correct it. In response to decreasing blood volume, the JMA release renin, which triggers the RAAS system that increase blood volume back to normal.
There are also low pressure receptors in the heart and lung, which are sensitive to increases in volume. They stimulate the release of ANP and BNP, which help the body to excrete urine.
The juxtaglomerular apparatus (JMA)
The juxtaglomerular apparatus (JMA) is a microscopic structure in the kidney that regulates the function of each nephron.
The JMA consists of three cells:
- macula densa, a part of the distal convoluted tubule of the same nephron - juxtaglomerular cells which secrete renin - extraglomerular mesangial cells
RAAS
The renin–angiotensin–aldosterone system is a hormone system that is involved in the regulation of the plasma sodium concentration and arterial blood pressure.
When the plasma sodium concentration is low or the renal blood flow is reduced, the juxtaglomerular cells in the kidneys convert prorenin (an intracellular protein) into renin, which is then secreted directly into the circulation. Plasma renin then cuts a short, 10 amino acid long, peptide off a plasma protein known as angiotensinogen. The short peptide is known as angiotensin I. Angiotensin I is then converted, by the removal of 2 amino acids, to form angiotensin II, by the enzyme angiotensin-converting enzyme (ACE) found in the endothelial cells of the capillaries throughout the body, within the lungs and the epithelial cells of the kidneys. Angiotensin II is a potent vasoconstrictor, resulting in increased arterial blood pressure. Angiotensin II also stimulates the secretion of the aldosterone from the adrenal cortex. Aldosterone causes the tubular epithelial cells of the kidneys to increase the reabsorption of sodium ions from the tubular fluid back into the blood, while at the same time causing them to excrete potassium ions into the tubular fluid which will become urine.
Angiotensin 2
Converted from angiotensin 1 in plasma by ACE. It has many effects on regulating blood pressure, volume, and osmolarity.
- It acts on a vasoconstrictor, increasing blood pressure.
- It stimulates the adrenal cortex to secrete aldosterone, which enhances NaCl reabsorption in the PT, TAL, DT, and CD.
- It stimulates ADH and thirst.
- Decreasing urine output.
Aldosterone
A steroid hormone produced in the zone glomerulosa of adrenal cortex. By stimulating expression of ion channels, it stimulates reabsorption of NaCl by the PT, TAL, DT, and CD. It also stimulate Na/K ATPase.
Half life 20 minutes.
Inhibits Renin in negative feedback.
RAAS (overal effect)
Responds to low blood volume by increasing NaCL absorption (via aldosterone). This increases the plasma osmolarity, which triggers the release of ADH, thereby increasing water reabsorption until osmolarity and blood volume return to normal.
Angiotensin 2 also increases blood pressure (by vascular constriction).
ANP/BNP
Atrial/Brain natriuretic peptide.
- Vasodilation of afferent and constriction of efferent, thereby increasing GFR.
- Inhibits renin secretion (thereby relaxing the afferent arterioles)
- Inhibits aldosterone production, thereby decreasing Na/Cl reabsorption by CD.
- Inhibits ADH secretion by posterior pituitary, there increasing urine excretion.
euvolaemia
The presence of the correct amount of blood in the body.
and hypo/hyper are termed accordingly
Causes of Na depletion -> hypovolemia
- Severe diarrhea
- Severe vomiting
- Blood loss
- Adrenal insufficiency (Addison’s disease)
Addison’s disease
An adrenal insufficiency. No aldosterone (hypoaldosteronism) reduces Na reabsorption, resulting in hypovolemia and coma. Treatment is cortisol which is a aldosterone precursor.
Causes of Na retention -> hyervolaemia
Chronic renal failure; kidney is not doing its job.
Heart failure; causes reduced renal perfusion, which triggers RAAS, which sparks Aldosterone to increase Na reabsorption and ADH to increase blood volume.
Hyperaldosteronism; excess adrenocortical hormones which increase Na reabsorption. May be caused by a tumor.
Why do patients with heart failure experience hypervolemia?
Heart failure causes reduced renal perfusion, which triggers RAAS, which sparks Aldosterone to increase Na reabsorption and ADH to increase blood volume.
Heart failure can also cause buildup up veinous pressure, which can lead to pulmonary and systemic edema. When this occurs in the lungs it causes shortness of breath.
They are therefore treated with diuretic drugs to reduce blood volume, pulmonary backup, and edema.
Renin
Synthesized as peprorenin, cleaved to prorenin which has little biological activity.
Renin is stored in juxtaglomerular cells of the kidney. Its only known function is to split angiotensinogen to angiotensin 1.
Renin regulation:
Stimulation:
- Decreased perfusion to kidneys
- Fall of arteriole pressure of JG cells
- Increased sympathetic activity
- increased circulatory chatecholamines (adrenaline)
Inhibitions:
- Increased Na/Cl absorption across macula densa
- Increased afferent arterial pressure
- ANP
- Angiotensin 2 (negative feedback)
Angiotensinogen, angiotensin 1, ACE, and angiotensin 2
Angiotensinogen: synthesized in liver. Cleaved by Renin.
Angiotensin 1: physiologically inactive. Cleaved by ACE.
Angiotensin Converting enzyme: cleaves a His-Leu from ang1, making ang2. It is in most endothelial cells.
Angiotensin 2: biologically active. T1/2 is 1-2 minutes. Causes vasoconstriction and high blood pressure. Acts on brain to stimulate secretion of ADH. Acts on adrenal cortex to secrete aldosterone.
