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Unit 10 > Week 2: Blood volume regulation > Flashcards

Week 2: Blood volume regulation Flashcards

1
Q

What is the main method that activates the RAAS system?

A

Decreases arterial pressure leads to decreases renal perfusion, this is sensed by mechanreceptors in the afferent arterioles of the kidneys.
This causes prorenin to be converted to renin and released from juxtaglomerular cells

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2
Q

What are the minor methods that assists the activation of the RAAS system?

A

Stimulation of renal sympathetic nerves
Beta 1 agonists such as isoprotenerenol

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3
Q

What drugs can be used to inhibit activation of the RAAS system?

A

Beta antagonists such as propanolol

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4
Q

What is the function of renin?

A

Enzyme
Catalyses the converions of angiotensinogen to angiotensin 1

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5
Q

What is the role of angiotensin 1?

A

Precursor for angiotensin 2.
ACE-1 enzymes in the lungs and kidneys will catalyse this conversion.

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6
Q

What drugs can stop the conversion of angiotensin 1 to angiotensin 2?

A

ACE-1 inhibitos - such as capropril

** not essential

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7
Q

What receptors does angiotensin 2 target?

A

AT-1 receptors
These are type 1 G protein coupled receptors

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8
Q

What is the function of iosartan?

A

Is a drug that inhibits AT -1 receptors, prevents the actions of angiotensin 2 at the target tissues

** not essential

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9
Q

What are the different sites of action for angiotensin 2?

A

The hypothalamus
The adrenal cortex
The kidney
The arterioles

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10
Q

What is the impact of angiotensin 2 in the adrenal cortex?

A

Acts on the zona glomerulosa cells
Stimulates the secretion and synthesis of aldosterone.

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11
Q

What is the purpose of aldosterone in RAAS system?

A

Acts on the principle cells of the renal distal tubule and collecting duct to increase Na+ reabsorption - hence water reabsorpttion.
This requires gene transcription and new protein synthesis hence the effects appear hours to days afterwards

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12
Q

What is the impact of angtiotensin 2 on the kidney?

A

Stimulates Na+ H+ exchange in the renal proximal tubule
Increases the reabsoprtion of Na+ and HCO3-

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13
Q

What is the impact of angiotensin 2 on the hypothalamus?

A

Increase thirst - hence water intake
Stimulates ADH secretion - increases water reabsoprtion in the collecting ducts.
Complement the effects of aldosterone on Na+ reabsoprtion

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14
Q

What is the impact of angiotensin 2 on arterioles?

A

AT-1 G protein receptor activates IP3, Ca2+ second messenger system
To cause vasoconstriction.
increase in total peripheral resistance leads to an increase in arterial blood pressure

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15
Q

What are the additional effects of angiotensin 2 not on blood pressure?

A

Pro-inflammatory
Pro-fibrotic
Pro-oxidatve stress
Pro-proliferative

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16
Q

What is the role of ACE2?

A

Enzyme acts to converte angiotensin 2 to Ang1-7
These have the opposite effects to angiotensin 2, causing vasodilation, anti-inflammatory, anti-fibrotic, anti-proliferative and anti-oxidative stress.

Are thought to be the receptors used by SARS-COV-2 in causing coronavirus disease

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17
Q

What is the relationship between increased blood pressure and improving cardiovascular function?

A

Increase in blood volume
Results in an increase in venous return
By Frank-starling mechanism this leads to an increased cardiac output.
This increases blood pressure.

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18
Q

What is meant by glomerular filtration rate?

A

The rate of filtration from plasma in the glomerulus capillaries to Bowman space.
Sum of all nephrons

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19
Q

What controls glomerular filtrate rate?

A

Starling forces
Hence is vulnerable to changes in mean arterial blood pressure

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20
Q

What equation demonstrates the factors influencing the glomerular rate of filtration?

A

GFR = filtration co-efficienct (Kf) [(GC hydrostatic pressure - BS hydostatic pressure) - reflection co-efficient (GC oncotic pressure - BS oncotic pressure)]

BS = Bowman space
GC = glomerular capsule
Pie symbol should be used for oncotic pressure
P for hydrostatic pressure

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21
Q

What is meant by reflection co-efficient?
How does this related to the kidney?

A

sigma symbol σ
Is a degree of impermeability.
Scored from 0-1 with 1 being impermeable

In a healthy GFR this is normally quite high due to negative charge of BM - this prevents proteins passing through the filter

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22
Q

What is meant by the filtration co-efficient?
How does this related to the kidney?

A

Symbol is Kf
Is high in most individuals as kidney glomerulus need to be very leaky in order to carry out their function.

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23
Q

Describe the starling forces that allows filtrate to cross out of the glomerulus into the Bowmans space.

A

Filtration co-efficient is high - very leaky to fluid
GC - higher hydrostatic pressure than the Bowmans capsule.
Glomerulus has a higher oncotic pressure than bowmans capusle, but this difference is smaller than the difference in hydrostatic pressure
Leads to an overall outwards force

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24
Q

What is the Bowmans capsule oncotic pressure?

A

Zero - in a healthy individual no protein should make it over the filtration barrier

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25
How is GFR kept within tight limits?
By autoregulation - not this is overruled when blood volume must change such as after haemorrhage or dehydration
26
How much plasma does the average kidney filter in aday?
180 L
27
How does the starling forces in the Glomerulus capillaries vary from the afferent to the efferent capillary?
Absolute oncotic pressure rises throught as no protein leaves the glomerulus but fluid is lost causing the concentration of protein to increase The hydrostatic pressure remains constant throughout due to autoregulation mechanisms to control renal blood flow.
28
What percentage of total blood flow goes to the kidneys?
25%
29
What equations should be used to calculated blood flow to an area?
Flow = Pressure / resistance
30
How can flow rate to the kidneys be altered?
Changing mean arterial blood pressure Alter resistance of the afferent and/or the efferent arteriole
31
What are the effects of changes in the diameter of the afferent arteriole on the GFR?
Dilation - increase hydrostatic pressure hence increase GFR Constriction - decrease hydrostatic pressure hence decrease GFR
32
What are the effects of changes in diameter of the efferent arteriole on GFR?
Constriction - increase hydrostatic pressure - lead to an increased GFR Dilation - decrease hydrostatic pressure - lead to a decreased GFR
33
What are the different factors that can alter to diameter of the afferent and efferent arteriole in the kidney?
Sympathetic nervous system Angiotensin 2 Atrial and Brain Natriuretic peptide (BNP and ANP) Prostaglandins Dopamine Nitric oxide
34
What are the effects of sympathetic nervous system on the diameter of the afferent and efferent arteriole?
Rapid onset of vasoconstriction Prioritise stabilising the mean arterial blood pressure at sacrifice of GFR (e.g after hemorrhage) Occurs by the renal sympathetic nerve activating alpha 1 receptors. Note there is a higher conc of alpha 1 receptors on the afferent arteriole so this constricts more leading to an overall decrease in GFR
35
What is the effect of angiotensin 2 on GFR?
Increase GFR Vasoconstriction of both afferent and efferent arterioles Efferent is more sensitive to angiotensin 2 than afferent. Low levels - conc of receptors does make a difference, increase GFR as efferent constricited more High levels - conc of receptors does not makes a difference = decreased GFR, as efferent fully constricted and afferent becomes constricted - effect as if only afferent being constricted.
36
What is the effect of Brain and atrial natriuretic peptide of GFR?
Known as ANP and BNP Dilation of afferent arteriole Constriction of efferent arteriole Dilatory effect is greater than constrictory effect Overall leads to an increase in renal blood flow as decreases renal resistance and an increase in GFR
37
What effect do prostaglandins have on GFR/ kidney function?
Produced locally in the kidney Cause vasodilation of both the afferent and efferent arteriole Protective of renal blood flow as often produced alongside sympathetic activation and angiotensin 2 This is very important, as opposes constriction to ensure renal failure does not occur. Maintain GFR Use of NSAIDs can be very dangerous if haemorrhage ocurs
38
What is the effect of dopamine on the GFR/kidney function?
Has a protective effect on renal function Dopamine is a precursor of norepinephrine Low level dilates cerebral, cardiac, splanchnic and renal arterioles but constricts skeletal and cutaneous arteries. Therefore low dosage has a protective effect on renal blood flow by helping to maintain renal blood flow - hence is often given after a haemorrhage
39
What are the effects of nitric oxide on GFR/ renal function?
Nitric oxide is synthesised by renal endothelial cells from L-arginine Causes dilation of renal arterioles This maintains GFR and increases renal blood flow to have a protective effect on the kidney Protects against vasoconstriction effects of the sympathetic nervous system
40
What substances can increase GFR?
ANP BNP
41
What factors have a negative effect on GFR and may lead to renal failure is not countered?
Catecholamine (sympathetic nervous system) Angiotensin 2 (high conc)
42
What are the key components of autoregulation of renal blood flow?
Myogenic response Tubuglomerular response
43
What is the myogenic response as a method of autoregulating the GFR?
Increased arterial blood pressure Stretch of vascular smooth muscles in afferent arterioles Activates stretch sensitive Ca2+ channels Cytosolic Ca2+ rises triggering contraction of smooth muscle. Results in Vasconstriction of afferent arterioles - increases resistance to blood flow
44
What is the mechanism of tubuloglomerula feedback in autoregulation of renal blood flow?
In high arterial blood pressure, glomerular flow and capillary pressure increases This increases GFR in a single nephron Increass delivery of NaCl to macula densa cells, these are osmoreceptors and secretes a vasoactive substance (adenosine) in response. Paracrine signalling triggers vasoconstriction of the afferent arteriole increasing resistance to flow and decreasing the renal blood flow Conversely in low BP, low Na+ detected by macula densa cells, trigger Juxtaglomerula cells to release renin. (tubuloglomerular feedback is simultaneously impaired)
45
Describe the relationship between blood pressure, renal flow and GFR.
Renal blood flow - self regulated over a wide range of MAP 80-180mmHg When blood pressure changes within this range RBF can be maintained by altering the resistance of the aterioles The resistance change is proportional to the change in pressure in order to maintain the same renal blood flow. If blood pressure falls outside this range autoregulatory mechanisms are no longer effective. Note regulation can be overrideen by extrinsic factors such as drugs.
46
What is meant by filtered load?
The amount of substance filtered into Bowmans space per unit of time
47
What equation is used to calculate filtered load?
FL = GFR x P[x] P[x] is the plasma concentration of x
48
What is the most important function of the kidney?
Reasborption of Na+ Is the major cation of the ECF, hence regulates blood volume and blood pressure Regulates effective arterial blood volume Na+ intake must be exactly equal to Na+ excretion
49
Describe the differences between na+ content an Na+ concentration and how this is relevant to the kidney/
Content - total amount in the body - determines ECF volume Concentration - content divided by ECF volume Kidney has separate mechanisms for water and sodium reabsoprtion, so one value may be normal and the other abnormal
50
What is meant by a positive Na+ balance? What are some consequences of this?
When Na+ intake is higher than Na+ excretion Leads to increase in ECF volume Causing high BP and odema
51
What is meant by Na+ balance in the kidney?
The levels of Na+ excretion by the kidney must be equal to the Na+ intake
52
What is meant by a negative Na+ balance and what are the consequences of this?
When the Na+ excretion is more than the Na+ intake Leads to a decrease in ECF volume, leading to low blood pressure.
53
What factors contribute to an Na+ gain?
Food Average diets contains more Na+ than needed (8g per day v 1.5-2.3 grams per day) Low Na+ diet triggers salt craving hence the diet plan is hard to follow
54
What factors contribute to a loss in Na+?
Small amounts lost in faeces Small amounts lost in sweat Urinary excretion balances the amount ingested
55
What happens to renal Na+ reabsorption in a Na+ loss?
100% of filtred load can be reabsorbed when Na+ intake is small
56
Give an overview of the role of different areas of the nephron in Na+ handling.
PCT - reabsorbed 2/3 (SGLT), here water follows TAL - 25% reabsorbed (NKCC2) - but no movement of water Early DCT - reabsorbd 5% and is water impermeable (NaCl cotranposter - gradient driven by Na+ K+ pump.) Late DCT and CD - reabsorbed 3% - fine tuning affected by aldosterone (ENaC)
57
What is meant by effective arterial blood volume?
EABV - the portion of the ECF contained within the arteries - is the volume that effectively perfuses the tissues
58
How do changes in ECF volume affect the effective arterial blood volume? What is the exception to this?
Normally are directly proportional, more ECF means greater volume in arteries Odemia is the exception - ECF volume increases but EABV decreases as majority of ECF is excessive filtration of fluid into the interstitial space
59
What factors affect the regulation of Na+ balance in the nephron?
Sympathetic nervous system ANP Starling forces in peritibular capillaries RAAS
60
How does the sympathetic nervous system activity affect the regulation of sodium balance?
Decrease GFR by vasoconstriction of afferent arterioles Results in increased PT reabsorption of Na+.
61
How does ANP effects regulation of Sodium balance in the nephron?
Causes vasodilation of afferent and vasoconstriction fo efferent arterioles - increase GFR leads to decreased Na+ reabsoprtion
62
How do starling forces (ECF volume) influence regulation of Na+ balance in the nephron?
Increased ECF volume decreases capillary oncotic pressure and inhibits Na+ reabsorption Decreased ECF volume - increased oncotic pressure and increased Na+ reabsorption
63
How does RAAS effect the regulation of Na+ balance in the nephron?
Angiotesin 2 stimualtes Na+ reabsoprtion in PT Aldosterone stimulates Na+ reabsorption in the late DT and CD
64
What is the response to increased Sodium ion intake?
1. Increased ECF and EABV Leads to all four of the following responses A. SNS activity decreases - arterioles remain dilated B. ANP production increases - results in dilation of afferent and contraction of efferent (high GFR) C. Decreased oncotic pressure in capillaries D. Decreased activation of RAAS Results in decreased reabsoprtion of Na+ in nephron
65
What is the response to decreased sodium ion intake?
Decreased ECF and EABV Leads to all four of the following responses 1. SNS activity increases - contraction of arterioles particularly afferent - decrease GFR 2. ANP production decreases - no vasodilative effect on arterioles 3. Oncotic pressure increases in the glomerulus 4. RAAS activation - aldsoterone effect of CD and angiotensin 2 effect on PCT Overall leads to decreased GFR and an increased resabsorption of Na+
66
What is the immediate response (seconds) to haemorrhage?
1. Baroreflex activates SNS and vasoconstriction to elevate BP 2. Neuroendocrine reflexes occur A. Physical and emotional stress causes catecholamine release from adrenal glands B. ADH is also regulated by baroreceptors C. Ang II is increased due to sympathetic activity to kidney Cause systemic vasoconstriction
67
What response to haemorrhage occurs within minutes?
Transcapillary refill - due to changes in the balance of Starling Forces Significant Blood loss causes a decrease in hydrostatic pressure , Oncotic pressure is greater than hydrostatic pressure - causes net movement into the capillary as fluid drains in from the interstitial fluid. This is self limiting and allows to gain about 0.5L in 30 minutes
68
What is the response to haemorrhage within hours?
Circulation volume is stabilised by increases renal Na+ and water reasborption. This effect can be mediated by angiotensin 2, aldosterone, SNS and ADH. Thirst and sodium appetite are also effected by baroreceptors and Angiotensin 2.
69
What causes ANP release?
Increased blood volume As consequence is increased Na+ excretion.
70
What is the response to haemorrhage after days?
Increased production of albumin, erythorcytes and platelets Replace the cellular functional components of blood to match the now restored blood volume
71
Give an overview of the distribution of phosphate in the body.
85% in bone matrix Rest 15% ICF and <0.5% ECF ICF - nucleotides, ATP and metabolic intermediates ECF - inorganic form and serves as abuffer for H+ 10% of phosphate in the plasma is protein bound
72
How is phosphate handled in the nephron?
Phosphate bound to protein remains in capillaries Free phosphate (90%) is filtered out 70% then reabsorbed in the PCT, 15% in PST This is accomplished by Na+-phosphate cotransporter in the luminal membrane of the proximal convoluted tubules
73
Give an overview of the distribution of calcium in the body
99% in bones 1% mainly in ICF (in bound form) and very little in ECF total plasma concentration is 5mEq/L
74
What regulates plasma Calicum ion concentration?
PTH
75
What form is calcium normally found in in the body?
40% bound to plasma protein 10% bound to anions such as phosphate and citrate 50% is free in the ionised form
76
Describe how Ca2+ may be handled in the nephron
99% of filtered is reabsorbed Is tightl coupled to Na+ reabsoprtion in the PT and LOH, but is different in the distal tubule
77
**Describe how Ca2+ is reabsrsobred in the PCT?
Paracellular by solvent drag And passive diffusion - dependent on intake of Ca2+
78
Describe how Ca2+ is reabsorbed in the thick ascending loop of henle?
paracellular - repelled by lumen positive potential difference creates by K+ secretion into lumen - driven by NKCC2 and K+ ion channel This is in close association with Na+ reabsorption by NCCK2
79
Describe why loop diuretics are useful in the treatment of hypercalemia and hypermagnesemia?
Loop diuretics inhibit Na+ reabsoprtion in the LOH by NKCC2, this reduces the conc gradient for K+ secretion back into lumen This decreases the lumen positive potential difference resulting in an equal reduction in Calcium ion absorption The same is true for magnesium ions
80
How is calcium ions reabsorbed in the distal tubule?
The site of Ca2+ reabsorpstion regulation Only site where not coupled to Na+ Is transcellular - apical membrane through Ca2+ ion channels which are increased by PTH, binds to calbindin in the cytoplasm, diffuse to basement membrane, leaves by active transport through Ca2+ ATPase ** extra reading
81
How is magnesium handled in the nephron?
80% of plasma Mg is free and can be filtered across, that bound to plasma proteins can not be. 95% reabsorbed and 5% secreted PCT - 30% reabsorbed (paracellular solvent drag) Thick AL - 60% reabsorbed - driven by luminal positive potential difference DT - 5% reabsorbed - transcellular through protein channels.
82
Describe how the hydrostatic pressure in the glomerulus remains constant from the afferent to the efferent arteriole.
Due to autoregulation mechanisms Only effective with a specific BP range
83
Describe what causes fluid to move from the bowmans capusle to the renal tubule
Filtrate enters the bowmans capsule Generates hydrostatis pressure - less than in the glomerulus - quantified as 15P this forces fluid from the capsule into the renal tubule.
84
What can the combined effects of hydrostatic and oncotic pressure in the GC and BS be called in relation to the driving force for filtration?
Pressure of urine filtration.
85
What is the impact on GFR is both afferent and efferent arterioles are constricted by an equal amount?
GFR remains the same.
86
What are the different structures found within the nephron?
1. Glomerular capillary and bowmans space 2. PCT 3. Proximal straight tubule 4. Thin descending limb 5. Thin ascending limb 6. Thick ascending limb 7. macula densa 8. DCT 9. connecting tubule 10. Cortical collecting duct 11. Outer medullary collecting duct 12. Inner medullary collecting duct
87
Describe the distribution of total body water.
66% ICF 33% ECF Of ECF 3/4 is interstitial and 1/4 is plasma
88
What factors have a protective effect for the kidney?
Prostaglandins Dopamine Dilating the afferent and efferent arteriole equally - this maintains blood flow to the kidney
89
Why should NSAIDs not be given to a haemorrhaging patient even if they are in pain?
NSAIDs - inhibit prostaglandin production PGE2 and PG12 normally have a protective effect on kidney function by dilating the afferent and efferent arteriole. Lack of PG leads to vasoconstriction of arterioles, this reduces the blood flow to the kidney - can cause kidney damage
90
What substances cause vasodilation of the afferent/efferent arteriole in the nephron?
Prostaglandins, Dopamine, Nitritix Oxide - dilate both equally ANP/BNP - dilate afferent only
91
What substances cause vasoconstriction of the afferent/efferent arteriole in the nephron?
ANP/BNP - constrict efferent only Cathecholamines/SNS - constrict both but constrict the afferent more Angiotensin 2 - constrict both, at low does have greater effect on efferent at high dose have greater effect on afferent
92
What is the function of autoregulatory properties of renal blood flow?
Protect the kidney from elevations or depressions in BP, that would effect renal blood flow, hence flow the glomerulus potentially causing damage to the filtration barrier.
93
What is the blood pressure range where autoregulation of renal blood flow can occur successfully?
80-180mmHg

Unit 10 (37 decks)

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