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