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

-Sympathetic Nervous System
-Anti-Diuretic Hormone
-Atrial Natiuretic hormone


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


What is angiotensinogen and where is it made?

-In the liver at a constant rate


Where is angiotensin I in high conc?



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


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


What is the aim of RAAS?

-To increase BP by increasing fluid volume


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



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


How does aldosterone reach the priciple cells?

-Can diffuse directly through cell membrane as steroid hormone


Why does an ACE inhibitor cause a dry cough?

-Decreased bradykinin in lungs as ACE breaks it down


What is bradykinin?



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


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


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

-ADH stimulates Na resorption in thick ascending limb through NKCC2


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


What is the general action of prostaglandins?



What effect do NSAIDs have on prostaglandins?

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


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


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


What is hypertension?

-Sustained increase in BP over 140/90


What is primary hypertension?

-Hypertension with no definitive cause


What is secondary hypertension?

-Hypertension secondary to disease eg cushings, chronic renal disease


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


What is Conn's syndrome?

-Hypertension and hypokalaemia caused by an aldosterone secreting adenoma


Why does pheochromocytoma cause hypertension?

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


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



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


How do L-type Calcium Channel blockers reduce hypertension?

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


How do a1-receptor blocers decrease hypertension?

-Reduce sympatheric tone by blocking NA


Describe non-pharmacological approaches to treating hypertension

-Stop smoking
-Reduce alcohol intake
-Reduced Na intake


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