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132 Cards in this Set

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What is Pressure diuresis?
The doubled increase in renal water output when arterial blood pressure rises only a few mm Hg.
What is Pressure natriuresis?
The doubled increase in renal SALT output when arterial blood pressure rises only a few mm Hg.
What is meant by the infinite feedback gain principle for renal control of longterm bp?
Whenever BP increases or decreases, the intake/output of water and salt will respond to return BP and levels to EXACTLY the equilibrium point.
What is the equilibrium point on the Renal output curve?
The point where normal sodium and water intake and output intersect and are equal.
What is the MAP for normal renal intake/output (equilibrium point)?
100 mm Hg.
2 determinants of the longterm arterial pressure level:
1. Degree of pressure shift of Renal Output curve for H2O/salt
2. Level of water/salt intake line.
What happens if either of the determinants of longterm MAP change?
BP will be regulated at a new level - the new equilibrium point.
What is MAP equal to?
What happens when TPR increases normally?
MAP increases, kidneys function normally, and MAP returns to normal within a few days.
Why doesn't an increase in MAP (caused by increased TPR) cause the equilibrium point for longterm BP control to shift?
B/c the resistance in the kidneys does not change even tho it does everywhere else; rather Pressure Diuresis/Natiuresis occurs.
What provides short term control of arterial blood pressure?
Sympathetic nervous system
How does the SNS control BP?
By effecting
-TPR and capacitance
-Cardiac contractility
How does the body control arterial pressure in the longterm?
By regulating body fluid volume
What determines the body fluid volume?
The balance between fluid intake and output
What is the Renal-Body fluid system for arterial pressure control?
When the body has to much ECF the blood volume and arterial pressure rise.
How does rising arterial pressure affect the kidney?
Causes it to excrete excess ECF to return pressure back to normal.
Pressure Diuresis:
Doubling of renal water output in response to increase in arterial pressure
Pressure natriuresis:
doubling of renal salt output in response to increase in arterial pressure
How has the renal-body fluid arterial pressure control system been refined over time?
By the addition of the renin-angiotensin mechanism
Renal output in a human at arterial pressure of 50 mmHg:
essentially zero
Renal output at BP = 100
Renal output at BP = 200
6-8 x normal
As urine output increases with increasing BP what else increases?
Sodium output - almost equally
3 variables that increase when you block the nervous pressure control mechanisms in dogs and then increase blood volume by infusing 400 mL blood:
-Cardiac output increases by 2X
-Urinary output increases by 12X
-MAP increases to 115mmHg above normal
What is the result of the increased urinary output after increasing a dog's blood volume?
CO and MAP both return to normal within one hour
What do we learn from the dog expirement?
The renal system is very capable of controlling MAP by changing volume output
How is renal regulation of MAP analysed?
By looking at the Renal Output Curve
What are the axes of the renal output curve?
X = arterial pressure
Y = intake/output of salt and water times normal
What does the equilibrium point on the renal output curve represent?
The MAP where salt/water output and intake are equal
What happens at MAP above the equilibrium point?
Water/salt output will increase to decrease MAP back to the equilibrium point
What will happen below the equilibrium point?
Water/salt will be retained until the MAP goes back up to equilibrium point.
Where is the normal equilibrium point for the renal output curve?
At 100 mm Hg - intake/output are 1
What happens if MAP goes up to 150 mm Hg?
Renal output increases to 3x normal until MAP goes back down
What happens if MAP goes down to 50?
Renal function is essentially zero
2 ways MAP can be increased:
1. Shift renal function curve to right toward a higher MAP level
2. Increase level of salt/water intake
What causes the renal output curve to shift to the right?
Abnormal renal functioning
We know that MAP = TPR x CO; doesn't that control MAP?
No; not in the long term.
What happens to MAP in the longterm if total body TPR is greatly elevated?
It will change CARDIAC OUTPUT
What happens to CO as TPR increases?
CO decreases
What controls the setpoint of MAP?
Renal function
Why doesn't increasing TPR increase MAP?
It does; but if the kidneys are functioning normally, then MAP will go back down in the longterm.
How is it that an increase in TPR and MAP doesn't increase the equilibrium setpoint for MAP on the renal function curve?
MAP increases everywhere EXCEPT in the kidney - there, pressure diuresis and natiuresis occur to reduce blood vol and MAP back to normal.
How does increasing ECF increase MAP directly?
1. Increase ECF
2. Increase blood volume
3. Increase Psf
4. Increase VR to heart
5. Increase CO
6. Increase MAP
How does increasing ECF increase MAP indirectly?
-Same steps to increase CO
-CO indirectly increases MAP by the autoregulation that responds to it to increase TPR; that then increases MAP.
so CO affects MAP in what two ways?
1. Directly increases MAP
2. Indirectly increases TPR via autoregulation -> increases MAP
2 reasons for why ECF volume increases as salt accumulates in the body:
1. Incr Salt -> incr fluid osmolality -> stim thirst center in brain -> drink more H2O -> ECF volume increases
2. Incr osmolality -> incr ADH release -> kidneys reabsorb more water/Na from renal tubules -> decr urine output, incr ECF volume
Where is ADH produced?
Hypothalamic-posterior pituitary gland
So what is the main determinant of ECF volume?
The amount of salt that accumulates in the body.
What 5 variables change in response to volume-loading hypertension?
-Blood volume
What is the basic cause of hypertension when sodium and water intake are markedly increased on day 0?
Increased cardiac output!
How does TPR initially respond to volume loading at day 0? Why?
It initially decreases -13% because of the baroreceptor acute response to decrease MAP.
How does TPR change over the next 14 days?
It increases secondarily as the autoregulation mechanism returns CO almost to normal.
What are the longterm results at day 14 after volume-loading?
-CO is almost back to normal (only increased by 5%)
-TPR is mrkdly increased by 33%
-MAP is elevated by 40%
What is it that causes MAP to stay elevated after volume loading?
Decreased renal functioning due to decreased renal mass; it changed the setpoint by shifting the renal function curve to the right.
How is increased TPR related to hypertension?
It does NOT cause it, but is a result of increased CO and the autoregulatory response trying to decrease it back to normal.
What are the longterm effects of volume loading HTN on blood volume and ECF volume?
Not that markedly elevated; thats because the MAP equilibrium point was increased by shifting the renal output curve to the right. That's the whole problem...
What levels of systolic and diastolic bp define HTN?
-Sys BP of >135
-Dia BP of >90
What is the response of TPR to acute increase in blood flow and MAP?
It increases so that bloodflow doesn't increase proportionately to the increase in MAP - to protect the vessels.
How does TPR change in chronic hypertension?
Even more to keep bloodflow lower as MAP keeps getting higher.
How does TPR continue to increase with chronic HTN?
By increasing the number of vessels (angiogenesis) and thickness of the vessel walls.
What is the chronic renal function curve determined by?
A balance of intrinsic and extrinsic factors
What are the 5 intrinsic factors within the kidney that determine the chronic renal function curve?
1. Physical factors (hydrostatic pressure)
2. Ang II
3. Prostaglandins
4. Kinins
5. NO from the renal medulla
What 5 extrinsic factors determine the chronic renal function curve?
1. SNS
2. Ang II
3. Aldosterone
4. Vasopressin (ADH)
5. ANP
Which factor that controls the chronic renal function curve is most important? Why?
Ang II by far - because it is the key controller of the body's adjustment to changes in water/salt intake and output.
The kidney's 2 mechanisms for controlling MAP are:
1. Changing ECF volume
2. RAS
What makes the RAS activate?
Decreased MAP - thekidney dects falling arterial presure in its afferent arteriole, and releases RENIN.
Where is Renin made and stored?
In juxtaglomerular cells in the kidney.
What are JG cells and where are they located?
Modified smooth muslce cells in the walls of the afferent arterioles just proximal to the glomeruli.
What happens to the renin released in response to decreased MAP?
It enters the blood and circulates throughout the body; some remains locally to initiate intrarenal functions.
What does renin do?
Acts on Angiotensinogen to release 10 AA peptide called Ang I
What does Ang I do?
Mild vasoconstrictor but not much.
How long does renin circulate?
Persists in blood for 30 min to 1 hr to cause more Ang I formation
What happens to Ang I? By what enzyme?
It gets 2 AAs split from it to form Ang II - done by ACE.
Where is ACE located?
Lung vessel endothelium
2 principal actions of Ang II:
1. Vasoconstriction all over the body
2. REnal retntion of salt/water
How long does Ang II persist?
only 1-2 min
What inactivates Ang II?
Where does most of the vasoconstriction caused by Ang II occur?
In arterioles (much less in the veins).
Result of vasoconstricting arterioles:
Increased TPR therefore increased MAP.
What happens when you induce hemorrhage enough to acutely decrease MAP to 50 mm Hg normally?
Pressure will rise back up to 83 mmHg when RAS is functional.
What happens when you induce hemorrhage enough to acutely decrease MAP to 50 mm Hg when RAS is nonfunctional??
Pressure will rise back up only to 60 mmHg
How long does it take the RAS to become fully active in acute hemorrhagic conditions?
About 20 min
2 Ways that Ang II causes the kidneys to retain salt/water:
1. Direct action on kidneys to cause salt/H2O retention
2. Causes adrenals to secrete ALDOSTERONE - which does same.
Function of Aldosterone:
Increased water and salt reabsorption by kidney tubules
How does the circulation of Ang II effect the renal function curve?
It causes MAP control setpoint to be at a higher MAP than normal (shifts the curve to the right).
How does Ang II directly cause water/salt retention in the kidney (4 ways)?
1. Constricts renal arterioles -> reduced bloodflow
2. Reduces post-glom cap pressure -> incr tubular fluid reabsorption
3. Decreases GFR
4. Directly causes tubular epithelium to increase Na reabsorption
Ang II is a powerful stimulator of:
Aldosterone secretion by adrenal glands
Important effect of Aldosterone is:
sodium reabsorption by the distal tubules
Result of increased sodium reabsorption:
Increased ECF volume, water retention, long term elevation of MAP.
At what MAP is the renal function curve equilibrium point if Angiotensin II level is zero?
75 mm Hg
At what MAP is the renal function curve equilibrium point if Angiotensin II level is 2.5X the normal level?
115 mm Hg
What would cause the renal output curve to shift to the left and make MAP 75?
Captopril - ACE inhibitors
What would cause the renal output curve to shift to MAP setpoint of 115?
-Direct effects of Ang II on the kidney
-Indirect effects acting through aldosterone
what is the RAS especially important in allowing us to do?
Eat more or less salt without really altering MAP.
How does the RAS let us eat more salt? (7 steps)
1. Increased salt intake
2. Increased ECF vol
3. Increased MAP
4. Decreased Renin / Ang II
5. Decreased H2O/Salt retention
6. Return ECF vol to normal
7. Return MAP to normal
How much does MAP rise in response to a 50-fold increase in salt intake?
No more than 4-6 mm Hg.
How much does MAP rise in response to the same salt intake increase when RAS is blocked?
MAP rises to 10X normal - like 50-60 mm Hg higher
How do Ang II levels change with increasing salt intake?
They decrease
How does the equilibrium point of the renal function curve change with increases in salt intake?
The curve does NOT shift to the right, but becomes steeper so that MAP is kept constant in spite of increased salt intake.
How soon does the direct action of Ang II on total body vasoconstriction take to occur?
How long does the indirect effect of Ang II to increase aldosterone take to occur?
Period of days
What is Goldblatt hypertension?
Induced HTN caused by removing one kidney and clamping the other renal artery to vasoconstrict it.
What is the kidney's response to a goldblatt clamp?
It senses reduced pressure in the renal artery beyond the constrictor, so thinks it should increase RAS to increase MAP.
How soon does Renin increase after putting the goldlbatt clamp on?
Within seconds - minutes.
What happens to MAP after placing the goldblatt clamp?
Ang II increases MAP DRASTICly over the first hour, then it continues to increase gradually over the next several days.
When does renin secretion peak and return to normal in Goldblatt hypertension?
Peak - within first hour
Return to normal - in 5-7 days
What causes renin secretion to return to normal when the goldblatt clamp is still on the kidney?
Ang II vasoconstriction and salt/water retention increased MAP, which increased renal arterial pressure, so Renin did not need to remain high.
In order to get the renal artery pressure back up (beyond the clamp), what had to happen to the rest of body MAP?
It increased to higher than normal levels - hypertension.
Why does the kidney care so much about having high enough pressure in the renal artery?
So that it can have adequete urine output - it doesn't care what MAP is, just its own.
2 increases in MAP are seen in goldblatt htn; what are they?
1. Direct effect of ANGII causing vasoconstriction
2. Indirect effect of Ang II and Aldosterone to incr Salt/H2O retention.
What happens to the renal output curve in Goldblatt hypertension?
It shifts to the right
Why does the RFC shift to the right in goldblatt HTN?
Because this is salt-insensitive - salt intake levels have not changed, but renal arteriole pressure has.
What happens to long term MAP:
-if you increase TPR
-if you increase renal artery P
TPR - will not increase MAP
Renal artery P - will increase MAP
How is mass balance of sodium and water achieved?
By reflex and hormonal response that effect the kidney
5 Reflex/hormonal responses to increased salt/water intake:
1. SNS activity decreases
2. ADH secretion decreases
3. Renin/angiotens system decr.
4. Aldosterone decreases
What type of feedback control is exhibited by the reflex and hormonal responses?
Proportionate - finite; they adapt and are good only for acute short-term responses.
What type of MAP controller is INFINITE feedback control?
The Renal-Body fluid controller - that is just the way that the kidney increases output in response to increase MAP and vice versa.
What is primary hypertension?
Aka essential; the cause is unknown but there are strong hereditary factors and obesity associations.
4 characteristics of primary HTN in obese patients:
1. Increased CO
2. Increased SNS activity
3. Increased AngII/aldosterone levels
4. Impared natriuresis
Why is natriuresis impaired in obese HTN patients?
Because the increased SNS activity causes increased renin release, increased AngII and Aldosterone, which PROMOTE salt/water RETENTION.
What is the difference between salt-sensitive and non-salt-sensitive HTN?
In a nonsalt-senstv HTN patient 3.5X normal salt intake will not change MAP; it will increase it in the salt-sensitive patient.
Why are some primary HTN patients salt-sensitive and some are not?
Due to functional differences in their kidneys - loss of nephrons or abnormal RAS functioning.
2 general drug classes used for treating HTN:
1. Vasodilators (to increase renal blood flow)
2. Natriuretic drugs to decrease tubular reabsorption of salt and water.
How is the difference between salt-sensitive and nonsalt-sens HTN exhibited on the renal function curve?
Both curves are shifted to the right, but only the salt-sens curve will show an increased MAP when salt intake increases.
What 3 mechanisms have the most acute response to changes in blood pressure?
1. baroreceptors
2. Chemoreceptors
3. CNS ischemic response
3 actions of the acute pressure change responses:
1. Vein constriction to incr VR
2. Incr HR and contractility
3. Periph arteriole constriction (incr TPR) to slow bloodflow and keep in capillaries longer
Within what timeframe do the acute response mechanisms operate?
Seconds to minutes
What 3 mechanisms have intermediate responses to changes in blood pressure?
1. RAS
2. Capillary fluid shift
3. Stress relaxation
How does capillary fluid shift respond to increased MAP?
More fluid shifts from CAPs -> tissues
When are the intermediate mechanisms most active?
Within 30 min to several hours
What is the longterm responder to changes in MAP?
The renal-blood volume pressure control response
Which pressure controller mechanisms have the highest feedback gain?
-Renal blood vol pressure control -> infinite
-Ischemic CNS response