Renal 4: Volume/Pressure Regulation Flashcards
What do RBF and GFR stand for?
Renal Blood Flow and Glomerular Filtration Rate
What’s the basic mechanism by which EC fluid is regulated?
The amount of Na+ excreted or absorbed
water follows sodium osmotically so changes in Na+ excretion - natriuresis - will alter water volume
Describe autoregulation of GFR and RBF
Autoregulation is the control using local variables. Such as restricting the afferent arteriole (More??)
What is Tubuloglomerular feedback?
Utilizes juxtaglomerular apparatus. Increased blood volume -> enhances tubular flow -> osmoreceptors in macula densa cells detect high levels of NaCl -> stimulate Na/K//Cl transporters -> macula densa cells release adenosine -> constricts afferent arteriole -> restore RBF and GFR (salt level!!! Not water)
What is the myogenic mechanism?
Vascular smooth muscle contracts in response to stretch and dilates in response to low pressure (baroreceptors!)
What 2 things influence the Starling forces that establish conditions for salt and water resorption?
- Neuroendocrine mechanisms: Angiotensin II, aldosterone, sympathetic activity, ADH, natriuretic peptides.
- Pressure natriuresis
What is Renin?
A protease released from JGA cells that converts angiotensinogen to angiotensin I.
What is ACE?
Angiotensin Converting Enzyme converts Angiotensin I to Angiotensin II
Where is ACE found?
On pulmonary and renal endothelial cell surfaces
What is the RAAS and what is it’s purpose?
Renin-Angiotensin-ADH-System. It promotes water and salt retention in response to a drop in BP
What are Angiotensin II’s direct fast actions (1-2 minute half life)?
- Constricts afferent arterioles to reduce RBF and GFR = less fluid out
- Constricts efferent arterioles: decreases hydrostatic and increases oncotic pressures in capillaries = more fluid absorbed
- Stimulates proximal tubule cells to reabsorb more Na+ and water
What are Angiotensin II’s slower, indirect actions?
- Releases aldosterone from the renal cortex
- Releases ADH from the hypothalamus
- Induces thirst from hypothalamus
What is aldosterone?
- trigger
- source
- action
- time frame
A lipid soluble steroid hormone (a mineralcorticoid excreted by adrenal cortex)
- Increases Na+ reabsorption and K+ secretion
- Up-regs Na+/K+ ATPases, Na+ channels and ATP levels in principle cells
- Fine tunes Na+ levels
- slower production in adrenal cortex (up regulation), longer latency and longer duration.
How does the efferent arteriole impact reabsorption?
CONSTRICTION = increased GFR and high tubular hydrostatic pressure; low vascular hydrostatic pressure, high vascular oncotic pressure: REABSORPTION of Na+ and water
DILATION = decreased GFR and low tubular hydrostatic pressure; high vascular hydrostatic pressure, low vascular oncotic pressure: EXCRETION of Na+ and water
Differentiate gross from fine regulation in the neuroendocrine regulation of reabsorption
Gross: 67% of filtrate in proximal tubule is reabsorbed DESPITE changes in GFR via glomerular tubular balance.
Fine: reg of Na+ levels and EC volume is carried out by neuroendocrine control of Na+ reabsorption in both the proximal and distal portions of the tubule .
What is the trigger of Angiotensin II?
A drop in blood pressure/volume (the Renin…etc)
What is the source of Angiotensin II?
Angiotensin I, which derives from Angiotensinogen synthesized in the liver.
What is the synthetic pathway of Angiotensin II?
Angiotensinogen converted by Renin into Angiotensin I; converted by ACE into Angiotensin II
What is the action of Angiotensin II?
- Vasoconstricts smooth muscle vasculature (afferent and efferent): increases resistance
- Causes Na+ reabsorption in PROXIMAL tubule
- Stimulates release of Aldosterone from adrenal cortex: reabsorp Na+ and water from DISTAL tubules
- Stimulates release of ADH from pituitary in hypothalamus: Water (only) reabsorp from COLLECTING DUCTS
- Induces thirst from hypothalamus: up intake
What are the actions of Angiotensin II on renal vasculature and tubules.
Constricts afferent arterioles: reduce RBF and GFR (less fluid out)
Constricts efferent arterioles: decreases hydrostatic and increases oncotic pressures in capillaries (more fluid reabsorbed)
Reabsorption of water and salt from convoluted tubules and collecting duct
What is the trigger and action of the sympathetic function in the kidney?
Trigger: drop is SYSTEMIC BP, emotional signals ie. fright
Action: baroreceptors detect drop, brain stem center activ symp neurons, postganglionic neurons innervate arterioles, JGA and tubular cells, release Renin …etc
How does ADH fit into volume control?
It is an anti diuretic hormone that up regs aquaporins, allowing the reabsorption of water (w/out salt). Regulates osmoregulation, etc
How does ANP inhibit reabsorption?
Atrial natriuretic peptides inhibits reabsorption by:
- Increase GFR by dilating the afferent arteriole
- Inhibit Na+ reabsorption by down reg Na+ channels
- Inhibit H2O reabsorption by reducing ADH release
- Inhibit secretion of renin and aldosterone
How does pressure natriuresis inhibit reabsorption?
Increase BP, more blood thru sys pushes out on vessel walls, shear stress causes release of NO, vessels dilate, altering g starling forces, gradient is not as steep, less reabsorption, more excretion!!
What is the relationship between pressure natriuresis and NO?
The increased pressure of the blood flow causes shear stress on vessel walls, causing NO release: vasodilator a vasa recta, increases capillary hydrostatic pressure which inhibits Na+ and water reabsorption
When is ANP and the other natriuretic peptides released, and what for?
In response to increased blood volume or pressure; work to reverse actions of RAAS
