Lecture 2: Regulation of Na+ and H2O Balance Flashcards
What is released by the kidneys that stimulated RBC production and affects blood volume?
Erythropoietin
Neurons responsive to changes in osmolality; activation causes release of?
Osmoreceptors; release of ADH
How sensitive are the osmoreceptors?
VERY sensitive, respond to change of 1 or 2 mOsm/kg
When osmoreceptors are faced with hyperosmolality, what happens?
Release of ADH, preventing further loss of water in urine, and stimulates thirst.
What molecules have the largest affect on the stimulation of ADH (vasopressin) secretion and thirst; which sugars via which method?
- Na+
- Sugars such as mannitol and sucrose when infused IV
How do increases in plasma osmolality caused by urea and glucose affect the secretion of plasma ADH levels?
Urea and glucose have little or no affect
What do arterial baroreceptors do?
Sense changes in the aorta and carotid arteries, sending afferent information to the brainstem vasomotor center, which then regulates CV and renal processes via autonomic efferents
How do cardiopulmonary baroreceptors work?
- Sense pressure in the cardiac atria and pulmonary arteries.
- Send afferent info in parallel w/ the arterial baroreceptors
There is some overlap in the cardiopulmonary and arterial baroreceptors, but which are the most important for ADH?
Cardiopulmonary baroreceptors have important influence on the hypothalamus, which regulates secretion of ADH
The binding of ADH to the V2 receptors causes what?
- Stimulates a Gs-coupled protein that activates adenylyl cyclase, in turn causing production of cAMP to activates Protein Kinase A
- Increases aquaporin-2 channel formation and apical membrane insertion, increasing H2O permeability of the collecting duct
How do the cortical collecting ducts compare to the medullary collecting tubules in regards to permeability?
Cortical collecting ducts - permeable to H2O at all times
Medullary - determined by the secretion of ADH, which is controlled by response of hypothalamic osmoreceptors
What is the major stimulus for ADH (vasopressin) secretion and thirst; what’s another stimulus?
- Increased ECF osmolarity (MAJOR)
- Decreased ECF volume (important for large changes in ECF volume/arterial BP)
The 2 cells of the JGA and their role?
1) Macula densa - the sensor!
2) Juxtaglomerular cells - secrete renin
If Na+ is high and fluid volume is low, what 2 things do the macula densa do?
1) Tell juxtaglomerular cells to release renin
2) Dilate the AFFERENT arteriole of the glomerulus (by secreting a little ADH)
The juxtaglomerular cells secrete renin in response to what 3 things?
1) Beta-adrenergic stimulation (sympathetics)
2) Decreases renal perfusion (in afferent arterioles - decreased glomerular hydrostatic pressure)
3) Signals from Macula Densa
What is the primary and secondary effects of the RAAS system?
Primary - maintain systemic BP
Secondary - Preserves the GFR
How does renin contribute to maintaining GFR?
- Renin converts angiotensinogen to angiotensin I, which is then converted by ACE to angiotensin II
- Angiotensin II promotes vasoconstriction of efferent arterioles which increases GFR
Angiotensin II promotes vasoconstriction of?
- Efferent arterioles = raises glomerular hydrostatic pressure
- All renal blood vessels and systemic vessels
Angiotensin II works to increase reabsorption of what, in which part of the kidney?
Reabsorption of Na+ and Cl- from the proximal tubule, in turn causing reabsorption of water.
Aldosterone is released from where in response to what?
- Released from Adrenal Cortex
- Increased plasma K+, decreased plasma Na+, or decreased BP
Where does aldosterone act?
Thick segment of the nephron loop, DCT, and cortical portion of collecting duct
A rise in plasma K+ stimulates the adrenal cortex to?
Increase its output of aldosterone, which in turn promotes the secretion and ultimate excretion/elimination of excess K+
The net effect of aldosterone is?
Conserve and increase water levels in the plasma by reducing the excretion of Na+, and thus water, from the kidneys
When osmolality of ECF increases what occurs to aldosterone?
A negative feedback loop will inhibit the release of aldosterone.
How does RAAS cause increased angiotensin
Angiotensin II promotes the release of Aldosterone from the adrenal cortex
What system opposes RAAS?
Blood pressure lowering system that involves - Atrial Natriuretic Peptide (ANP)
Where is ANP produced and what does it promote?
Produced in atrial cardiac muscle cells and promote excretion of large amounts of Na+ in the urine
The main action of ANP is what and happens in what part of the nephron?
Directly inhibit Na+ reabsorption in the distal parts of the nephron, thus increasing Na+ excretion and accompanying osmotic H2O excretion in urine
What 2 things does RAAS inhibit?
1) Inhibits renin secretion by the kidneys and acts on the adrenal cortex to inhibit aldosterone secretion
2) Inhibits secretion and actions of ADH
What affect does ANP have on the smooth muscle of afferent arterioles?
Inhibits them causing relaxation (vasodilation) and increasing GFR —> Increases Na+ and H2O filtration
Hyponatremia describes a state where?
- Plasma Na+ concentration is lower than normal
- Body fluids are diluted and cells swell from decrease osmolality
What is a consequence of hyponatremia?
Cerebral edema and hypovolemia
SIADH causes excessive release of what, leading to?
Excessive ADH, leading to excessive H2O retention, cells swell, and increased Na+ secretion (major cause of low Na+ levels)
What causes:
urine > serum osmolality
serum > urine osmolality?
Urine > Serum = SIADH
Serum > Urine = Water intoxication
What is the difference between nephrogenic and central diabetes insipidus?
Central: Decreased secretion of ADH
Nephrogenic: Kidney resistance to ADH
The administration of ADH will, in moderate to severe cases raise urine osmolality and lower the urine volume by more than 50% in which kind of diabetes insipidus?
Central Diabetes Insipidus
Causes of central diabetes insipidus?
1) Head trauma
2) Pituitary tumor
3) Neurosurgery
Causes of nephrogenic diabetes insipidus?
1) Lithium toxicity
2) Renal disease
3) Hypokalemia
4) Pregnancy
