Blood Pressure And The Kidneys

Question 1

What is the major electrolyte of ECFV?

Answer 1

→ Na

Question 2

If you add Na+ to the blood why doesn’t hypernatremia happen (Increase in Na+ concentration)?

Answer 2

→ If Na+ increases

→ an equivalent amount of water is drawn with it

Question 3

Equation for BP?

Answer 3

→ CO x TPR

Question 4

What does an increase in blood volume lead to?

Answer 4

→ ventricular filling and increased stroke volume (Starlings law)
→ Increase cardiac output
→ Increase blood pressure

Question 5

What is long term control of blood pressure?

Answer 5

→ regulating Na levels

Question 6

What is short term control of blood pressure?

Answer 6

→ Baroreceptors

Question 7

Flow chart for changes in Na balance

Answer 7

Changes in Na balance
↓
Changes in osmolarity
↓
ADH release
↓
H2O moves through ADH stimulated aquaporin channels in collecting duct

Question 8

Why does resuscitation fluid not cause hypernatremia?

Answer 8

→ It is isotonic
→ Na+ cannot cross cell membranes
→ fluid will expand the ECFV

Question 9

What is the effect of retained sodium the same as?

Answer 9

→ adding isotonic fluid
→ It draws an equivalent amount of water with it
→ Increase in blood pressure

Question 10

How is Na+ sensed in the body?

Answer 10

→ Indirectly
→ A change in ECFV occurs (up or down)
→ Stretch and pressure receptors in CVS detect this

Question 11

What are the afferent pathways for detecting indirect changes in Na+?

Answer 11

→ Cardiac volume receptord
→ Baroreceptors
→ Renal arterial pressure

Question 12

What are the efferent pathways for responding to changes in Na+?

Answer 12

→ Neuronal : sympathetic nervous system
→ Hormonal : RAAS, ANP
→ Haemodynamic : + or - GFR, pressure natriuresis

Question 13

How is sodium taken in the body?

Answer 13

→ Diet 10 to > 400 mMol a day

Question 14

How is sodium removed from the body?

Answer 14

→ Sweat/faeces

→ Regulated renal excretion

Question 15

What are mammals designed to do with Na+?

Answer 15

→ Conserve sodium

Question 16

What is the Na+ conserving system called?

Answer 16

→ RAAS

Question 17

How does RAAS work?

Answer 17

1) A loss of blood pressure stimulates the secretion of renin
2) Renin acts on a liver substrate called angiotensinogen and converts it to angiotensin I
3) Angiotensin I is converted to angiotensin II by angiotensin converting enzyme ( epithelial cells of the lung)
4) Angiotensin II acts on the AT1R receptor on the adrenal cortex and stimulates it to release aldosterone
5) Increases Na+ reabsorption in the nephron and increases K+ secretion
6) vascular smooth muscle contracts (vasoconstriction and BP increases)

Question 18

Where is the macula densa?

Answer 18

→ The region of contact between the afferent arteriole and the distal tubule of the same nephron

Question 19

What are renin secreting juxtaglomerular cells?

Answer 19

→ Modified smooth muscle cells along the afferent arteriole

Question 20

What is renin secreted in response to?

Answer 20

1) decrease in BP and blood volume and renal blood flow detected by afferent arteriole mechanoreceptors
2) decrease Na levels at the macula densa
3) Sympathetic nerve activation of beta 1 adrenoceptors

Question 21

What is aldosterone and where is it synthesized and what is it released by?

Answer 21

→ Steroid hormone
→synthesized in the zona glomerulosa of the adrenal gland
→ released by the action of angiotensin II

Question 22

What does a decreased amount of Na+ at the macula densa mean?

Answer 22

→ Decreased GFR

Question 23

Where does aldosterone act?

Answer 23

→ Nuclear receptors mainly on DCT cells

Question 24

Where is Na+ and water mainly reabsorbed?

Answer 24

→ PCT

Question 25

How does aldosterone increase Na+ retention?

Answer 25

→ increases the expression of eNAC channels | → Increases activity of Na+/K+ pump

Question 26

Where is the eNAC found?

Answer 26

→ Luminal side of the collecting duct

Question 27

How does the Na+/K+ pump work to retain Na+?

Answer 27

→ Na+/K+ pump actively pumps sodium out → Low intracellular concentration of Na+ → creates a diffusion gradient from the lumen of the tubule of the DCT → Na+ diffuses in via the eNAC → Na+ does not stay in the cell because the Na+/K+ pump is taking the Na+ out

Question 28

What is Na+ absorption coupled with?

Answer 28

→ K+ excretion

Question 29

What does excess aldosterone result in and why?

Answer 29

→ Hypokalaemia → K+ into the cell via Na+/K+ pump → K+ passively diffuses out of the cell into the lumen of tubule

Question 30

Where are ANP and BNP found?

Answer 30

Specialized cardiac myocytes

Question 31

What are ANP and BNP released in response to?

Answer 31

→ Increased cardiac filling pressures

Question 32

What are the renal effects of ANP?

Answer 32

→ Increased natriuresis ( Na+ excretion) | → Diuresis (H2O excretion)

Question 33

What are the vasculature effects of ANP?

Answer 33

→ Vasodilation by stimulation of PKG in vascular smooth muscle cells → Decrease systemic BP

Question 34

What are the hormonal effects of ANP?

Answer 34

→ Decrease renin secretion | → Decreased aldosterone secretion

Question 35

What is the main effect of ANP?

Answer 35

→ opposes RAAS | → Na+ excreting system

Question 36

What is pressure natriuresis?

Answer 36

→ Increase in Na+ renal excretion due to a rise in renal arterial pressure

Question 37

What is the relationship between pressure and Na+ excretion?

Answer 37

→ The higher the pressure the higher the concentration of Na+ in the urine

Question 38

How does pressure natriuresis occur?

Answer 38

→ A rise in medullary capillary pressure → causes an increase in fluid filtration and interstitial pressure → Prevents tubular reabsorption

Question 39

Why is GFR not involved in pressure natriuresis?

Answer 39

→ Renal arterial pressure does not increase GFR | → Due to powerful renal auto-regulation

Question 40

What are the criteria for hypertension?

Answer 40

→ Diastolic > 90mmHg | → Systolic > 140 mmHg

Question 41

What are the classifications of hypertension?

Answer 41

→ Secondary - identifiable cause | → Essential - unknown cause ( > 90% of cases)

Question 42

What do secondary causes of hypertension involve?

Answer 42

→ Excess Na+ reabsorption and abnormalities in hormone secretion → Liddle's syndrome → Conn's syndrome → Renal artery stenosis

Question 43

What can essential hypertension involve?

Answer 43

→ Abnormal handling of Na+ balance

Question 44

What is Liddle's syndrome?

Answer 44

``` → Autosomal mutation that is rare → Genetic form of high blood pressure → Increases eNAC activity → Increases renal Na+ retention → Suppresses aldosterone/ renin ```

Question 45

What are the effects of Liddle's syndrome?

Answer 45

→ Increased ECFV | → Increased BP

Question 46

What is Conn's syndrome caused by?

Answer 46

→ Overproduction of aldosterone by the adrenal gland tumor

Question 47

What are the consequences of raised aldosterone?

Answer 47

Acts on principal cells lining CD → Increase in ECFV → Renal sodium reabsorption increases → Increase eNAC / ATPase/ K+ excretion → decrease in renin secretion

Question 48

What are the consequences of Addisons disease?

Answer 48

``` → Insufficient release of aldosterone → Chronic Na+ loss → Decreased ECFV → Severe hypotension → Collapse and death ```

Question 49

How does renal artery stenosis cause Na+ retention?

Answer 49

``` Decrease in renal artery pressure due to stenosis ↓ Decreased blood flow ↓ Renin secretion ↓ Angiotensin II production ↓ Increased aldosterone ↓ Increased vasoconstriction ``` This effect is systemic so it would affect the other kidney and the nonstenosic kidney will reduce renin production

Question 50

How does congestive heart failure cause oedema?

Answer 50

``` LV failing to maintain enough pressure to maintain perfusion ↓ Arterial baroreceptors deactivated ↓ Body thinks blood volume is decreased ↓ Activates sympathetic output ↓ Increase RAAS system ↓ Stimulates Na+ retention ↓ ECFV expands ↓ Less arterial pressure ↓ Less hydrostatic pressure ```

Question 51

What are environmental factors that can cause essential hypertension?

Answer 51

→ Life style → Diet → Diabetes

Question 52

How is ECF volume sensed?

Answer 52

Change in amount of sodium in ECF Atrial stretch receptors, Arterial baroreceptors Afferent arteriole NaCl delivery to DT RAAS – sodium-retaining ANP – sodium-excreting Change in renal sodium and water excretion

Question 53

How is RAAS activated by? How is aldosterone secretion increased by?

Answer 53

Reduced renal perfusion Increased sympathetic activity Aldosterone secretion is increased by RAAS Increased plasma [K+]

Question 54

Describe the difference between aldosterone effect on principal and intercalated cells

Answer 54

``` →Increases Na/K ATPase →Increases expression of ENaC channels on luminal membrane →Resulting in Increased Na+ reabsorption Increased K+ secretion ``` ``` Acts on intercalated cells of CD →Increases H+ ATPase- which expells H+ into tubule →Resulting in →Increased H+ secretion →Increased HCO3- reabsorption →Bicarbonate will move into the ECF Metabolic alkalosis ```

Question 55

Defences against volume depletion

Answer 55

RAAS Normal, continuous adjustment of Na excretion and ECF volume →Can reduce Na excretion to very low levels in hypovolemia​ in distal tubule ADH →Last line of defence against volume depletion →Non-osmotic ADH secretion if BP drops by ≈ 10-15%- ADH secretion is increased regardless of plasma osmolarity →RAAS is already fully activated