Control of Plasma Volume Flashcards
What fluid do you add to increase the ECF volume - explain why this works
Add isosmotic fluid
Isosmotic fluid will not penetrate into the ICF as it has the same osmolality as the plasma -> will only distribute itself amongst the ECF
What is pressure natriuresis and pressure diuresis. What do they cause
Pressure natriuresis - increased Na excretion
Pressure diuresis - increased water excretion
They cause the ECF volume to decrease -> decrease BP
What are the types of reabsportion and secretion
Paracellular - solutes go through gap junctions which are loose enough to allow solutes through
Transcellular - solutes travel through the cells lining the lumen
What are the functions of tight junctions
Prevent movement of ions out of the interstitium into the lumen
Maintain cell polarity by preventing movement of ion channels from the apical to basolateral membrane and vice versa
What are aquaporins and what aquaporins are found where
AQP - protein channels that allow the movement of water into and out of cells
AQP1 - found in PCT and descending loop of Henle. Is always expressed
AQP2,3,4 - found in the collecting duct. Can be recruited if more water needs to absorbed -> can add or remove these AQP depending on ADH
How is Na reabsorbed in the nephron - name some of the channels/tranporters used and what transporter drives Na reabsorption
Na is reabsorbed transcellulary and is driven by basolateral N-K-ATPase which creates a concentration gradient in the cell
Transporters:
- Na-H antiporter
- Na-glucose symporter
- Na-AA co-transporter
- NKCC2 symporter
- NaCl symporter
- ENaC
What two presures drive water movement from the interstitium into the capillaries
Hydrostatic pressure - generated by water in the interstitium. Hydrostatic pressure is high -> drives water into capillaries
Oncotic pressure - generated by proteins in capillaries and assists the movement of water into capillaries
Describe the movement of solutes from the PCT (not Na)
- Glucose, AA and lactate are removed first from the PCT
- Bicarbonate removed next
- Then phosphate removed
- Finally Cl is removed down its concentration gradient
What channels and structures are found in the S1 part of the PCT
Basolateral N-K-ATPase
Na-H exchanger
Na-glucose/AA/phosphate/carboxylic acid co-transporters
Aquaporin 1
What channels and structures are found in S2-3 parts of the PCT
Basolateral N-K-ATPase
Na-H exchanger
Aquaporins
Cl transport is via transcellular and paracellular reabsorption
Describe the structure of the descending limb of the loop of Henle
Descending limb is formed of squamous epithelium
Has lots of aquaporins -> very permeable to water
Few transporters -> no reabsorption of Na -> concentrated filtrate forms as water leaves but solutes don’t
Describe the structure of the ascending limb of the loop of Henle
Ascending limb is cuboidal epithelium
Split into thick and thin AL with thick AL having lots of transporters to move ions from the filtrate into the capillaires
Cells in thick AL have lots of mitochondria for active transport
Describe the transporters found in the thick AL
NKCC2 transporters
N-K-ATPase
ROMK - allows NKCC2 transporters to continue to function
How does Na reabsorption in the thick and thin AL differ
Na reabsorption in the thin AL is passive as water absorption in DL creates gradient for passive Na reabsorption
Na reabsorption in thick AL is active - requires transporters
Describe the differences between DCT1 and DCT2
DCT1 only has NCC transporters on its apical membrane
DCT 2 has both NCC transporters and ENaC on its apical membrane
Greater amount of Cl reabsorbed in DCT2 as the ENaC are not electroneutral and cause the filtrate to become negatively charged -> drives paracellular Cl reuptake
What diuretic blocks NCC transporters and what diuretic blocks ENaC
Thiazide blocks NCC
Amiloride blocks ENaC
What two cell types are found in the collecting duct
Principle cells
Intercalated cells - type A and type B
What is the function of principle cells in the collecting duct
Reabsorb Na via ENaC
This drives Cl uptake as it causes the lumen to become negatively charged
What are the functions of intercalated cells
Type A - secretes H+ -> acid secreting. Aids in regulating acidity and alkalinity of plasma. Express H+-ATPase and H-K-ATPase
Type B - secretes HCO3- -> bicarbonate secreting -> regulates alkalinity. Express Cl-HCO3--ATPase
What physiological mechanisms occur during hypotension to increase the BP to normal
Stroke volume is increased via dopamine - increases contractility of the heart
Vasoconstriction of arterioles in the body increases the TPR
RAAS
SNS stimulates mechanisms to increase the BP
ADH release - inserts AQP into the membranes of DCT and collecting ducts to increase water retention
What does the SNS stimulate during hypotension
Increased SV
Renin release/RAAS activation
Na reabsorption
Vasoconstriction
Vascular hypertrophy
What are the effects of the RAAS system
Increase SNS activity
Tubular Na, Cl reabsorption, K excretion and water retention
Aldosterone secretion
Arteriolar vasoconstriction
ADH secretion
What does aldosterone stimulate
Upregulates N-K-ATPase in DCT cells
Upregulates Na channels in CD and colon
Stimulates K secretion into tubule
Stimulates H+ secretion into CD
Upregulates Na/Cl co-transporters in DCT
Stimulates Na and water retention in the gut, salivary and sweat glands
How does stimulation of RAAS result in generalised oedema - what loop is created
Positive feedback loop is created
Renin release is stimulated by decreased renal perfusion
Angiotensin II causes increased SNS activity
Increased SNS activity cuases increased vasoconstriction resulting in decreased renal perfusion
Decreased renal perfusion results in more renin release
What is the pressure-natriuresis curve
Curve that shows the threshold pressure required for Na excretion
In hypertension, baroreceptors reset themselves to a higher pressure -> need higher BP to excrete same amount of Na
Name some causes of hypertension
Liver disease
Underlying hypertension
Fear - white coat effect
Kidney disease
CVS disease
Pain
Hyperaldosteronism
Sleep deprivation
Fluid overload
Diet - high salt diet
Drug effect
