Exam 10 - Long Term Control Of BP Flashcards
If MAP increases….what happens to local flow?
- adjust to bring back down to normal flow
- due to short and long term responses
Long term control of BP
- keeps MAP constant over course of life
- tied into control of ECF volume and CBV
- movement of body fluid driven by solute concentration
- osmotically active salutes = anything impermeable
- proteins / electrolytes / etc.
Increase CBV increases pressure via 3 ways:
- Increased volume in arteries/veins -> up pressure
- if no change in compliance - Up VR -> up preload -> up SV -> up CO -> up pressure
- if no change in SVR - Up CO -> up flow -> up auto reg -> up constriction -> up SVR
- > up pressure
- response to mechanism two
- > up pressure
- Decrease in CBV is just the reverse
Small change in CO can cause:
- large change in BP
- 5-10% increase in CO can raise MAP 50 mmHg
Increase in CBV will do what to MAP
- Increase
- Kidneys increase urine output
- decrease reabsorption of H2O/Na
- reverse is true
Control of fluid and salt output
- done by kidneys
- water follows salt
- kidneys can bring MAP back to baseline
Normal fluid intake
2300 ml/day
- 200 via metabolism
- 2100 via ingestion
Normal fluid output
2300 ml/day
- 100 via sweat
- 100 via feces
- 700 via respiratory tract/skin
- 1400 via urine
Renal output
Renal filtration - renal reabsorption
Factors affecting filtration
- MAP
- Renal blood flow
- Pressure in glomerular caps
- constrict afferent = down filtration
- constrict efferent = up filtration
- oncotic pressure in glomerular caps
- increase causes decrease in filtration
- hemodilution increases filtration
Factors affecting reabsorption
- [ angiotensin II ]
- Aldosterone
- ADH
- all will increase reabsorption
Renal-Body fluid system response to increase in MAP
- increase filtration and/or decrease reabsorption
- water/salt output > intake
- decreased CBV
- MAP decreases until back to original level
- Reverse is true
Pressure Diuresis (acute changes)
- Kidneys have highest critical closing pressure
- will close before all other organs
- If MAP changes…CBV will move up or down to match water/salt intake
- difficult to change long term MAP w/o changing renal output curve or intake curve
What will cause a chronic increase in MAP
- decreased renal function
- increased salt intake
What if long term change in SVR
- Kidneys will bring MAP back to normal via CBV
- Problem if change in renal resistance…
- this decreases renal function and MAP will go up
Renin-Angiotensin System
- in play when pressure goes down
- Prorenin (produced/stored in juxtaglomerular cells)
- splits into renin -> released into afferent arterioles and circulates
- renin in blood 30-60 minutes…acts on angiotensinogen
- releases angiotensin I (mild vasoconstrictor)
- carried to lungs where ACE turns into angiotensin II
- ACE also in epi cells of renal tubules and periph vessels
- Ang II lasts for 1-2 min then deactivated by angiotensinase
Angiotensin II
- potent vasoconstrictor on arterioles/minor on veins (minutes)
- changes SVR - increased water/salt reabsorption (days)
- causes adrenal glands to release aldosterone
- increases water/salt reabsorption - WILL shift renal function curve to right…increase MAP
Salt tolerance in normal renal function
- if Kidneys normal / renin secretion normal…
- person salt insensitive
- Renin-angiotensin system allows us to change salt intake and keep same MAP
Normal salt intake
1500 mg or 25 mEq per day
Walter vs Salt Intake
- easier to excrete water
- increase salt -> stimulate thirst center/hypoth and post pit
- thirst center -> increase water intake -> increase ECF volume
- hypoth and post pit -> up ADH -> up reabsorption -> up ECF
- increase in salt intake creates more change in CBV than water
Hypertension
- MAP > 110….trending down (d>90….s>135)
- shortens lifespan
- causes: volume loading / renin-angiotensin imbalance / constriction
- can be primary (known) and essential (unknown)
Diuretic curve shit
- shift renal curve left
Coarctation of aorta
- clamp-like obstruction distal to arch
- kidneys perceive lower pressure than normal
- increase angio II…distal becomes normal…proximal high MAP
- flow remains normal due to local control
Preeclampsia
- increase MAP in pregnancy
- decreases filtration rate
- decreases release of vasodilators
Neurogenic hypertension
- caused by strong stimulation of sympathetic
- anxiety, excited, etc.
Neurogenic hypertension via baroreceptors
- baroreceptors cut off
- over activation of vasomotor center
- cannot inhibit vasomotor center
Essential hypertension
- 90-95% of cases
- obesity account for large risk (65-75%)
- weight loss and exercise is treatment
- increase in CO / sympathetic / angiotensin II and aldosterone /
- impairment of renal function….need to give drugs too
Treatment: lifestyle / vasodilator drugs / reabsorption block drugs- drugs target renal arterioles….make Kidneys think up in BP