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Flashcards in Week 4 - Control of BP Deck (32):
1

What are the 4 mechanisms of long-term control of blood pressure?

-Renin-Angiotensin-Aldosterone-System
-Sympathetic Nervous System
-Anti-Diuretic Hormone
-Atrial Natiuretic hormone

2

Where is renin released from? What 3 mechanisms stimulate its release?

-Granular cells of JGA
1)Reduced NaCl in DCT detected by MD ->Cause afferent arteriole to release PGs ->PGs cause granular cells to release renin
2)Reduced perfusion pressure detected by baroreceptors in afferent arteriole
3)Sympathetic stimulation of JGA

3

What is angiotensinogen and where is it made?

-Precursor
-In the liver at a constant rate

4

Where is angiotensin I in high conc?

-Lungs

5

What are the functions of angiotensin II?

-Stimulates aldosterone production from adrenal cortex
-Stimulates Na resorption in PCT (stimulate NHE)
-Stimulates vasoconstriction of afferent and efferent arteriole to decrease GFR and thus decrease excretion

6

Describe the pathway of aldosterone stimulation by RAAS

-Angiotensinogen->Angiotensin I by renin
-Angiotensin I ->Angiotensin II by Angiotensin Converting Enzyme
-Angiotensin II stimulates aldosterone

7

What is the aim of RAAS?

-To increase BP by increasing fluid volume

8

What is the main angiotensin II receptor? What type of receptor is it?

-AT1
-GPCR

9

Describe the actions of aldosterone on the kidney

-Acts on principle cells of collecting duct and stimulates Na and thus water resorption
-Increases expression of ENaC and NaKATPase and apical K channel

10

How does aldosterone reach the priciple cells?

-Can diffuse directly through cell membrane as steroid hormone

11

Why does an ACE inhibitor cause a dry cough?

-Decreased bradykinin in lungs as ACE breaks it down

12

What is bradykinin?

-Vasodilator

13

Explain how the sympathetic nervous system stimulates renin release from JGA

-In response to low bp, High levels of sympathetic stimulation reduces renal blood flow via vasoconstriction of the arterioles
-This causes a decrease in GFR and thus a decrease in the filtration fraction
-This causes less Na to be delivered to DCT which is detected by MD of JGA
-MD causes afferent arteriole to release prostaglandins which cause vasodilation and stimulates the release of renin from granular cells

14

In what 3 ways does the sympathetic nervous system reduce Na excretion

-Directly acts on PCT to activate NHE and NaKATPase
-Causes vasoconstriction of afferent arteriole to reduce GFR -> reduced Na Excretion
-Stimulate Renin release from JGcells

15

How does antidiuretic hormone act as a long-term regulator of BP?

-ADH stimulates Na resorption in thick ascending limb through NKCC2

16

How does atrial natiuretic peptide act as a long-term regulator of BP?

-ANP acts to reduce bp by promoting Na excretion and thus water excretion
-ANP (which is sythesised and stored in atrial myocytes) is released from atrial cells in response to stretch -> Increased blood volume -> increased SV -> increased stretch
-When corculating vol reduced -> less stretch -> less ANP released
-ANP acts as a vasodilator of afferent arteriole which increases renal perfusion = increased GFR = increased excretion
-ANP also inhibits Na reabsorption along the nephron

17

What is the general action of prostaglandins?

-Vasodilator

18

What effect do NSAIDs have on prostaglandins?

-Inhibit cyclo-oxygenase pathway involved in prostaglandin synthesis -> decreased PGs

19

What is the danger of adminstering NSAIDs in Acute Kidney Injury?

-Further increase the injury by inhibiting PGs and causing a reduction in renal blood flow -> decreases GFR further

20

What effect does dopamine have on the BP?

-Dopamine formed locally in the kidney from L-DOPA
-Acts on dopamine receptors on renal BVs and cells of PCT and TAL
-Causes vasodilation and increases renal blood flow
-Causes reduces reabsorption of NaCl by inhibiting NHA and NaKATPase

21

What is hypertension?

-Sustained increase in BP over 140/90

22

What is primary hypertension?

-Hypertension with no definitive cause

23

What is secondary hypertension?

-Hypertension secondary to disease eg cushings, chronic renal disease

24

How does renovascular disease cause hypertension?

-Occlusion of renal artery/renal artery stenosis causes a fall in perfusion pressure
-Decreased perfusion leads to an increase in renin
-Increase in renin results in an increased aldosterone
-Increased Na and Water reabsorption -> Hypertension

25

What is Conn's syndrome?

-Hypertension and hypokalaemia caused by an aldosterone secreting adenoma

26

Why does pheochromocytoma cause hypertension?

-Excess production of NA and A
-Increased action of sympathetic nervous system
-Increased vasoconstriction -> Hypertension

27

What is the eqn for calculating BP? What is the eqn for calculating CO?

-CO x TPR
-CO=SV x HR

28

How is hypertension treated pharmacologically?

-ACE inhibitors
-AngIIR antagonists
-Thiazide Diuretics or Spironolactone
-L-Type Ca Channel blockers
-a1-receptor blockers
-b-blockers if previous MI

29

How do L-type Calcium Channel blockers reduce hypertension?

-Reduce Ca entry into vascular smooth muscle of cells
-Relaxation of vascular smooth muscle

30

How do a1-receptor blocers decrease hypertension?

-Reduce sympatheric tone by blocking NA

31

Describe non-pharmacological approaches to treating hypertension

-Diet
-Exercise
-Stop smoking
-Reduce alcohol intake
-Reduced Na intake

32

What is the short-term regulator of BP? Explain it

-Baroreceptor reflex
-Baroreceptors are stretch receptors located in aortic arch and the carotid which adjust symp and parasymp input to the heart to alter CO and adjust symp input to vessels
-They are sensitive to pressure. Increased pressure on the receptors causes increased signals to be sent to the medulla -> increased parasympathetic input -> decreased CO and TPR
-Decrease in blood pressure decreases signals sent to medulla -> decreased parasymp and increased symp (if needed) and vasoconstriction occurs