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Urinary System > Lecture 5.1: Renal Control of Volume and Blood Pressure > Flashcards

Lecture 5.1: Renal Control of Volume and Blood Pressure Flashcards

1
Q

What is included in Extracellular Fluid (ECF) Volume?

A

• Intravascular Volume
• Interstitial Fluid Volume

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2
Q

What is the clinical presentation of too much ISF?

A

Oedema

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3
Q

Where is most of the blood in the body?

A

• Most blood is in the veins

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4
Q

What is Frank-Starling’s Law?

A

• Cardiac Output = Stroke Volume x HR (Where
SV = EDV-ESV)
• End Diastolic Volume (EDV) & End Systolic
Volume (ESV)
• i.e. more in → more out

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5
Q

“For a given level of vascular capacity, the ‘fullness of the circulation’ and the rate of venous return vary directly with the volume of blood”

A
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6
Q

What happens to venous pressure if blood volume increase?

A

It increases

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7
Q

What effect will increased venous pressure have on cardiac output?

A

Increases cardiac output

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8
Q

What is Blood Pressure (BP)? What is a normal reading?

A

• Force exerted by blood against vessel walls
• Less than 120/80 mmHg

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9
Q

What is the Mean Arterial Pressure Equation?

A

Mean arterial pressure = cardiac output x total peripheral resistance (TPR)

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10
Q

What is BP influenced by? (5)

A

1) Cardiac factors: volume of blood from left ventricle contraction
2) Peripheral resistance: arteriolar diameter, which is variable
3) Blood volume: total volume of blood (i.e. cells and plasma) if blood volume ↓
BP ↓
4) Viscosity: ↑ blood viscosity causes greater resistance to flow and therefore ↑
arterial pressure
5) Arterial elasticity: when the elasticity of larger arteries ↓, resistance ↑, and
therefore systolic pressure ↑

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11
Q

Why do the kidneys require a stable mean arterial blood pressure?

A

• The kidneys require a stable mean arterial blood pressure to maintain GFR (i.e.
BP must not be too high nor too low)

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12
Q

Why must GFR remain constant? What rate?

A

• To maintain renal function and prevent renal damage
• Approx. 120 ml/min/1.73 m2)

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13
Q

What mechanism is the GFR maintained by?

A

• Autoregulation (see Session 3)

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14
Q

How is Blood Pressure Regulated?: Short Term

A

• Autonomic Regulation
• Baroreceptor Reflex
• Respond to Vascular Stretch (see CVS Unit)
• Adjust sympathetic input to peripheral resistance vessels to alter TPR
• Adjust sympathetic and parasympathetic inputs to the heart, to alter cardiac
output

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15
Q

How is Blood Pressure Regulated?: Long Term

A

• Extracellular Fluid Volume
• Renin Angiotensin-Aldosterone System (RAAS)

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16
Q

What organ is primarily responsible for maintaining BP long term? How?

A

• The kidneys primarily control long-term BP by
controlling the amount of Na+ in the ECF

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17
Q

How many grams of sodium does WHO recommend a limit of?

A

2g/day

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18
Q

Obligatory Reabsorption of Na+ in PCT: Percentage? How?

A

• 65% of filtrate
• Basolateral Na+/K+-ATPases and luminal Na+ channels (e.g. ENaCchannels and
SGLT2 co-transporters)

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19
Q

Obligatory Reabsorption of Na+ in TAL of the Loop of Henle: Percentage? How?

A

• 25%
• Na+/K+/2Cl- co-transporter

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20
Q

Variable Reabsorption of Na+ in Distal Tubule: Percentage?

A

• Up to 8%

21
Q

Variable Reabsorption of Na+ in the Outer Medullary Collecting Duct: Percentage?

A

• Up to 3%

22
Q

What percentage of Na+ is excreted in the urine?

A

• c.0.4%

23
Q

What percentage of Water is Reabsorbed in the Proximal Tubule?

A

• 65%

24
Q

What percentage of Water is Reabsorbed in the Descending Thin Limb of the
Loop of Henle?

A

• 15%

25
Q

What percentage of Water is Reabsorbed in the Collecting Duct?: Water-Loading and in Dehydration

A

• 5% (during water-loading)
• >24% (during dehydration)

26
Q

Thick Ascending Limb (TAL) (late segment): Ion Movement [Transporters]

A

• The Na+/K+/2Cl- co-transporter ‘dilutes’ the tubular fluid by moving Na+/K+/2Cl
into the tubular epithelium of the TAL
• K ions then diffuse back via the renal outer-medullary potassium channel
(ROMK) into the tubular lumen to maintain Na+/K+/2Cl- co-transporter activity
• The return of K maintains a positive charge in the TAL lumen, allowing the
paracellular reabsorption of Na+, Ca2+ and Mg2+from the TAL.

27
Q

What is the role of Loop Diuretics such as Furosemide (in regards to TAL)

A

Loop diuretics, such as furosemide, block the Na+/K+/2Cl- co-transporter by competing for Cl-

28
Q

Distal Convoluted Tubule Transporters

A

Na+/Cl- enter across apical membrane via the electroneutral NCC transporter (Sodium-chloride symporter)

29
Q

What Hormones and Diuretics is the NCC Transporter sensitive to?

A

• Thiazide diuretics
• Parathyroid hormone
• Calcitriol/Vitamin D3 (stimulate Ca2+ reabsorption via apical Ca2+ channels,
and a Vitamin D3-dependent protein)

30
Q

What type of cells make up the majority of the distal nephron?

A

Principal Cells

31
Q

What transporter/channel on Principal Cells is responsible for water reabsorption?

A

• Reabsorption of water via AQP-2

32
Q

What transporter/channel on Principal Cells is responsible for Na+ reabsorption?

A

• Principal cells reabsorb 2-3% of total filtered Na+ions via ENaCs (epithelial Na+
channels)

33
Q

What hormone promotes ENaC expression?

A

• Aldosterone promotes ENaC expression
• Allowing maximal Na+ reabsorption during volume depletion

34
Q

What diuretic blocks ENaC?

A

Amiloride is a ‘K+-sparing’ diuretic that acts by blocking ENaC

35
Q

Na+ moves without Cl- in the ENaC inhibitor, what effect does this have on the lumen of the collecting ducts?

A

Here, Na+ moves without Cl-, making the lumen more negatively charged, thereby promoting the electrogenic secretion of K+ via selective K+ channels

36
Q

What sensors are involved in regulating ECF volume? (3)

A

• The Juxtaglomerular Apparatus (JGA)
• The Atria
• The Carotid Sinus

37
Q

What are Effector Mechanisms?

A

Mechanisms that respond by altering Na+ excretion and systemic vascular resistance

38
Q

Sensors involved in Regulation of Volume: The Juxtaglomerular Apparatus (JGA)

A

The granular cells of the JGA release renin in response to low BP, thereby initiating the renin-angiotensinaldosterone system (RAAS)

39
Q

Sensors involved in Regulation of Volume: The Atria

A

They release natriuretic peptides to promote Na+ excretion

40
Q

Sensors involved in Regulation of Volume: The Carotid Sinus

A

Regulates the activity of the sympathetic nervous system, and relays the hypovolemic stimulus to vasopressin

41
Q

What is the process of Renin release from Juxtaglomerular Apparatus (JGA) ?

A

• In response to ↓ BP, the biologically-inactive precursor (prorenin) within the
granules of the granular cells is cleaved to form renin
• The active enzyme renin is then released from the granular cells that surround
the afferent arteriole, into the circulation (T1/2 80 minutes)

42
Q

What is the role of Renin?

A

Renin’s only known function is to cleave angiotensinogen (renin substrate), to form angiotensin I

43
Q

What is Angiotensin (II)?

A

Angiotensin is a hormone that helps regulate your blood pressure by vasoconstriction and triggering water and sodium intake

44
Q

Regulation of Renin Secretion: Stimulation (3)

A

• Low BP (sensed by cardiopulmonary baroreceptors) triggers sympathetic
stimulation & catecholamine release to stimulate β1 receptors in JGA
• Low BP (sensed by afferent arteriole baroreceptors) stimulates local release of
prostaglandins
• Increased sympathetic activity via renal nerves

45
Q

Regulation of Renin Secretion: Inhibition (4)

A

• Increased Na+/Cl- reabsorption by the macula densa cells of the early distal
tubule
• Elevated BP in the afferent arteriole
• Angiotensin II (Negative-Feedback)
• Vasopressin

46
Q

How is Angiotensin II formed? What effect does it have on the Kidneys and BP? (6 Steps)

A

• Angiotensinogen (453 aa protein formed by the liver)
• Renin the cleaves this into Angiotensin I
• Angiotensin-Converting Enzyme (ACE) converts this to Angiotensin II (active)
• Angiotensin II stimulates Aldosterone release (from adrenal cortex)
• Aldosterone causes increased Na+ absorption in kidneys (direct and indirect)
• ↑ ECF Volume ↑ systemic BP

47
Q

Effect of Aldosterone on Sodium uptake?

A

• Released from the zona glomerulosa (a mineralocorticoid)
• Causes sodium to be absorbed and potassium to be excreted into the lumen
by principal cells
• Acts on the cells of the DCT and cortical collecting duct by stimulating the
expression of ENaC channels

48
Q

If BP rises too much due to Renin, what hormone stimulates a decrease in BP?

A

Atrial Natriuretic Peptide (ANP)

49
Q

Where is Atrial Natriuretic Peptide (ANP) produced? How does it work?

A

• Heart Atrial Cells
• ANP inhibits expression of ENaC channels in the principal cells
• ANP block Renin secretion
• This reduces Na+ reabsorption from the connecting tubules/collecting ducts
• Thus causing ↓ ECF volume and ↓ BP

Urinary System (15 decks)

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