Session 4 - Changes in plasma volume

Question 1

What is the intracellular and extracellular conc of: a) sodium b) potassium c) calcium d) Chloride

Answer 1

a) i - 15 e - 140
b) i - 140 e - 5
c) i - 0.0001 e - 2.5
d) i - 5 e - 100

mM units

Question 2

Does osmolarity in the PCT change? Explain.

Answer 2

• Osmolarity remains the same throughout the PCT
• Chloride ion reabsorption lags behind in order to ensure osmolarity remains the same.
• Water is taken with the glucose, AA, and lactate to prevent changes in osmolarity.

Question 3

What happens to the concentration of the solute as it moves from the PCT to the loop of Henle

Answer 3

Goes from isomotic to hypotonic

Question 4

What does the ascending and descending limb of the loop of henle do?

Answer 4

• Descending limb absorbs water making the solution very hypertonic
• Ascending limb absorbs ions making solution hypotonic (Thick ascending limb impermeable to water)

Question 5

How does the thin ascending limb reabsorb sodium ions

Answer 5

via paracellular route

Question 6

How does the thick ascending limb reabsorb sodium ions?

Answer 6

Luminal side:

1) NAKCC2 - na, k and 2 Cl into cell
2) ROMK - potassium out of cell

Apical side:

1) Cl transporters
2) Na - k - ATPase

Question 7

How does the descending limb reabsorb water?

Answer 7

paracellularly

Question 8

How does the early and late DT reabsorb sodium and calcium ions?

Answer 8

luminal:

1) NCC transporter - Na and Cl symporter
2) Calcium transporter

Apical:

1) Cl transporter
2) NCX - Calcium into ECF and sodium into cell
3) Na - k - ATPase

Question 9

What ion is the DCT a major site for reabsorption of?

Answer 9

calcium

Question 10

What are the 2 cell types in the late DCT and CD? What are their functions?

Answer 10

1) Intercalated cells - active reabsorption of chloride and secretion of H+ or HCO3 to make urine acidic or basic
2) Principal cells - Variable water uptake through aquaporin dependent on the actions of ADH

Question 11

Give the equation for BP

Answer 11

BP = CO x TPR

Question 12

Give the equation for CO

Answer 12

CO = SV x HR

Question 13

How is the BP regulated in the short term? How does this mechanism regulate BP?

Answer 13

Short term regulation – baroreceptor reflex, nerve endings in the carotid sinus and aortic arch sensitive to stretch:

o Adjusts sympathetic and parasympathetic inputs to the heart to alter CO

o Adjusts sympathetic input to peripheral resistance vessels to alter TPR.

Question 14

Describe the function of the RAAS and how it works. What factors affect the release of renin? Where is it released from?

Answer 14

Renin released from granular cells of Juxtaglomerular apparatus (JGA) 3 factors affect release from JGA:

1. Reduced NaCl delivery to distal tubule – achieved by decreased circulating volume
2. Reduced perfusion pressure in the kidney causes release of renin – sensed by baroreceptors in afferent arterioles of glomerulus
3. Sympathetic stimulation to JGA increases release of renin

Process of the RAAS:

Angiotensinogen – produced by liver circulates in blood and becomes angiotensin I, cleaved by renin 2.

Angiotensin I becomes angiotensin II by ACE 3.

Angiotensin II: —> Vasoconstricts afferent and efferent arterioles, decreasing GFR –> Stimulates sodium reabsorption at PCT, stimulates NA-H exchanger in apical exchanger –> Increases thirst sensation, –> Stimulates aldosterone release from adrenal cortex.

Aldosterone activates ENaC, apical K channels, and Na/K/ATPase, stimulating Na and therefore water reabsorption. Hormone crosses intracellular membrane and increases expression of these channels.

Question 15

What are the 2 types of angiotensin 2 receptors available?

Answer 15

AT1 and AT2

Question 16

What are the actions of bradykinin? What breaks it down?

Answer 16

Bradykinin has vasodilator actions and is broken down by ACE

Question 17

How can the sympathetic nervous system autoregulate renal blood flow?

Answer 17

• High levels of sympathetic stimulation reduce renal blood flow by vasodilating blood vessels to muscles, decreasing GFR and Na excretion.
• This activates apical NaCl cotransporter and basolateral Na/K ATPase in DCT
• This stimulates renin release from JG cells, leading to increased Ang II levels and increased aldosterone levels.

Question 18

How does ADH autoregulate BP? Where does it act?

Answer 18

• Forms concentrated urine by retaining water and increasing sodium reabsorption and controlling plasma osmolarity
• ADH release stimulated by increase in plasma osmolarity or severe hypovolaemia.
• Acts on thick ascending limb to stimulate apical Na/K/Cl co transporter.

Question 19

What is the function of natriuretic peptides (ANPs)?

Answer 19

• ANP (atrial NPs) promotes sodium excretion and is released from atrial cells in response to stretch
• Low pressure volume sensors in the atria inhibit ANP if there is a reduced effective circulating volume.
• ANP actions:

o Vasodilates the afferent arteriole and increases blood flow, therefore increasing GFR o Inhibits Na reabsorption

Question 20

Why should NSAIDs be avoided if someone has compromised renal blood flow?

Answer 20

Prostaglandins:

• Act as vasodilators and enhance GFR, and reduce Na reabsorption.
• Helps to maintain renal blood flow and GFR in presence of vasoconstrictors
• NSAIDs inhibit COX pathway involved in forming prostaglandins and therefore giving NSAIDs when renal perfusion is compromised can further decrease GFR and lead to acute renal failure.

Question 21

What are the 2 types of hypertension?

Answer 21

Essential and secondary

Question 22

How can you treat hypertension? Give 3 methods

Answer 22

1) Treating the cause in secondary hypertension,
2) ACE inhibitors,
3) Diuretics (decrease circulating volume)
4) L-type calcium channel blockers – relaxes vascular smooth muscle
5) Beta blockers to reduce effects of sympathetic output on heart
6) Exercise, diet, reduced alcohol and na intake