Exam3Lec4Sodium/Potassium/ElectrolytesBalance Flashcards
A decr in GFR leads to a ____ in Na+ excretion
decrease
What can change with decreased blood pressure?
Filtration presure
What is the equation for GFR?
GFR = Kf [PGC - PBC) - piGC ]
What two hormones incr Na+ reabsoprtion?
Aldosterone and
Angiotensin II
What type of hormone is Aldosterone and Angiotensin II?
Aldosterone: steroid hormone
Angiotensin 2: peptide hormone
Does atrial natriuretic peptide (ANP) and BNP favor sodium reabsorption?
NO, its favors sodium excretion
Which organ secretes aldosterrone and what is the fxn of aldosterone>
Adrenal gland secretes aldosterone and the fxn of aldosterone is to incr sodium reabsoprtion in the kidney
Aldosterone incr Na+ Reabsorption in what segments of the nephron?
Late Distal Tubule and Collecting Duct
Explain how aldosterone incr Na+ reabsorption
- In the presence of Aldosterone, it stimulates the activation of the Na+ channel (ENaC) on the lumen side.
- Once Na+ enters cytosol through the channel, aldosterone also incr activation of the sodium potassium pump to incr Na+ into the intertisum.
note that Na+ enters cytsol through a sodium channel that IS NOT voltage gates, just diffuses through the endothelial sodium channed (ENaC)
How is angiotensin 2 formed?
- Liver synthesizes Angiotensinogen and is excreted into the bs
- Angiotensinogen is then turned into Angiotensin 1 by the renin enzyme.
- Angiotensin 1 is then turned into Angiotensin 2 by ACE enzyme.
renin chops off the last 4 aa from Angiotensinogen to become angiotensin 1
ace removes 2 more aa from angiotensin 1 to beceom angiotensin 2
What are 4 mechanisms of which angiotensin 2 can incr Na+ reabsorption
- incr Aldosterone
- decr Kf (surface area)
- incr Proximal Reabsorption directly
- incr Filtration Fraction (FF)
Angiotensin II is a very powerful ____ hormone
vasoconstricting
How does Angiotensin II incr filtration fraction (FF)?
Angiotensin II constricts both afferent and efferent arterioles but has more effect on efferent arteiole
You incr vasoresistance through vasoconstrition lowering plasma flow
Because angiotensin II can increase Filtration what occurs to the GFR and RPF?
GFR remains unchanges and RPF decr
You incr vasoresistance through vasoconstrition lowering plasma flow
GFR remained unchanged b/c both aff and eff are constricted
As a result of angiotensin 2 incr Na+ reabsoption, does the protein osmotic pressure incr or decr in peritubular capillaries and why?
It’s increased bc there is more plasma flow in GFR is filtered into proximal tubule. Lots of proteins are left behind inside the glomerular capillary so the protein osmotic pressure incr,
What leads to the release of ANP (atrial natriuretic peptide) ?
Volume expansion of the heart leading to atrial stretch leads to the atrial cell releasing ANP
What are the two main effects of ANP?
- Vasodilation leading to lowering of blood pressure
- Incr Na+ and H2O excretion
does both simultaneously
action s mediated by cGMP
Similar Structures of the Natriuretic Peptides Family
Where is ANP found?
Atria and other tissues
has 1 disulfide bond
Similar Structures of the Natriuretic Peptides Family
What is BNP? Where is it found?
BNP is an isoform of ANP. It is found in the brain, atria, and ventricles.
Why is BNP important clinically?
It is an important indicator to assess the health of the heart. If someone has heart failure, they can look at BNP lvls
Similar Structures of the Natriuretic Peptides Family
What is CNP? Where is it found?
CNP is an isoform of ANP. It is found in the CNS and vasculature
Atrial Natriuretic Peptide (Factor)
ANP (ANF) ____ Na+ Reabsorption
Decreases
oppostire
How does ANP/ANF/BNP decr Na+ reabsoprtion?
ANP/ANF/BNP incr cGMP activity and this inhibits Na+ reabsorption through inhibiting the sodium channel so Na+ comes in less,
Actions of Atrial Natriuretic Peptide is mediated by?
cGMP
Explain the action of Actions of Atrial Natriuretic Peptide
when the blood volume incr
A decr in protein osmotic pressure leads to what?
Increases Na+ Excretion
(glomerulus)
remember: GFR = Kf [PGC - PBC) - piGC ]
Decreased Protein Osmotic Pressure Increases Na+ Excretion (glomerulus)
How does a decreased Protein Osmotic Pressure increase Na+ excretion in the Proximal Tubule?
It lowers osmotic pressure in the PT capillary so less Na+ is reabsorbed back into the capillary and you see an incr is Na+ excretion/
How does sympathetic innervation (epi and norepi) effect absorption?
It increases Na+ reabsoprtion
Sympathetic incr increases Na+ reabsorption through which structures?
- Arterioles
- JG cells
- Kf (surface area)
- Tubule
How does sympathetics (norepi or epi) incr Na+ reabsorption through the tubules?
it increases the active Na/K APTase by activating PP1 and thus increase Na reabsorption.
Angiotensin 2 has a similar effect but different receptor.
Increased blood flow to cortex results in?
Increased Na+ excretion
Is the juxtamedullary nephron salt sparing or salt wasting?
Salt sparing
because it has a longer loop of henle and they are more efficent in Na+ reabsoption
Is the cortical nephron salt sparing or salt wasting?
Salt wasting
b/c they don’t reabsorb as much, bc shorter tubule less, sa for reabs
What is pressure natriuersis/diuressis and what is it caused by?
Pressure natriuresis/diuresis is an increase of Na+ /water excretion
Caused by an increase in arterial pressure in the absence of a change in renal blood flow and glomerular filtration rate.
During pressure natriuresis/diuresis , In the range of autoreg, there is a wide range of change (incr) in arterial pressue, no change in RBF or GFR, and there is NO autoregulation of urine outflow leading to a large incr of urine outlflow. Why does this possibly occur?
possibly Because there is inhibition of Na+ and H2O reab in the proximal tubule
hypothesis is thar an incr bp inhibiits antiporter (Na+/H+) decr Na+ reab
What is this curve?
Renal functional curve
if you have some Na or H20 retention, this can make your BP incr pass the equilibrium point then you kidney reaction incr alot, so you see incr excretion of H2O and salt (outake>intake) to lower back to equilibrium
What does this graph represent?
Renal functional curve of someone with hypertension. The curve shifted to the right, so their equiibrium point incr.
Pts with HTN have to operate in high BP in order to achieve that equilibrium
What is Liddle syndrome?
an autosomal dominant disorder characterized by early, and frequently severe, hypertension associated with low plasma renin activity, metabolic alkalosis due to hypokalemia, and hypoaldosteronism.
What causes liddle syndrome?
This syndrome is caused by disregulation of an epithelial sodium channel (ENaC) due to a genetic mutation. It does not breakdown/degrade fast enough so you have accumulation of sodum reabsoption. The increased sodium reabsorption leads to hypertension
Review: ADH ____ tubular permeability to water
Incr
remember: by phosph AQP2 it makes the whole tubule water perm. In the absence of ADH the channels are recycled and the apical membrane is again impermeable to water. It does this regulation at the corticla and medullar collecting duct
Primary control of H2O excretion by ____.
ADH
Primary control of H2O excretion is by ADH, what is the exception?
osmotic diuresis
For osmotic diuresis, the reabsorption of water is dependent on what? Increased solute excretion nearly always results in what?
- The reabsorption of water is dependent on the reabsorption of solutes.
- Increased solute excretion nearly always results in increased urine flow
EX: (diabetes): so much glucose is being processed through tubule and it cannot reabsorb all of it so by the time it leaves the proximal tubule, glucose is left behind and receptors are sat, and its excreted in urine. B/c glucose has high osm , when you excrete glucose you take H20 with it.
For osmotic diuresis, is the reabsorption of solutes dependent on the reabsorption of water?
NO
The reabsorption of water is dependent on the reabsorption of solutes.
What stimulates and inhibits ADH secretion/release?
- Stimulated by: ATII
- Inhibited by: ANP
Secretion of ADH is stimulated by physiological factors, other hormones and drugs
You have a patient with hypertension who you have been treating with a loop diuretic for 1 month. His initial
plasma [K+] was 4.5 mEq/L and has decreased to 3.0 mEq/L.
How much potassium has the patient lost ?
Potassium Intake = 100 mmoles/day
PotassiumExcretion = 100 mmoles/day
90% urine 10% feces
lost 21 mmol
things to note: intake=output. Pt lost plasma K+ so ECF was lost, ICF unchanged.
Regulation of Potassium Excretion
100% of the filtered K+ is reabsorbed by the time it reaches what segment of the nephron?
the beginning of the distal tubule
late distal and collecting duct is primarily K+ secretion
What is the effect of aldosterone intake on potassium excretion?
Increase aldosterone intake daily, you excrete more K+.
Those who start with a high plasma K+ concentration will always have high postassium excretion independent on K+ concentration. why? Aldosterone increases K+ Secretion &
K+ Stimulates K+ Secretion directly
Aldosterone ____ K+ secretion and ____ stimulates K+ secretion ____
Aldosterone increases K+ Secretion &
K+ Stimulates K+ Secretion directly
this is occuring at the distal tubule and cortical collecting duct
more K+ in plasma drives K+ pump. K+ pump is more active. incr in K+ secretion
What aldosterone stimulate simultaneously?
It simultaneously stimulates Na+ reabsoption and K+ secretion.
presecne of aldosterone stimulaates Na+ channel and you have a lot more Na+ comein is, this stimulates the Na+K+ pump and more Na+ is reabsorbed.
You have a patient with hypertension who you have been
treating with a loop diuretic for 1 month. His initial
plasma [K+] was 4.5 mEq/L and has decreased to 3.0 mEq/L.
Why would a diuretic cause hypokalemia ?
- Drugs like furosemie (loop diuretic) i can inhibit the reabsorption of Na+K+and 2Cl- by inhibiting the cotransporters located in the thick ascending limb. K+ would be excreted b/c its not getting reabsorbed
- Aldosterone can incr Na+ reabsorption and incr K+ secretion
- Drugs like thiazied can specifically inhibit NaCL cotransporters in the distal convulated tubule. So you see more sodium traveling through the tubule, and once it reaches the distal tubule and cortical collecting duct, Na+ stimulates aldosterone regulation mentioned in number 2. So you see that K+ is stimulated for secretion
- see an incr of Na+and K+ INSIDE tubule
What controls phosphate excretion and Ca2+ absorption?
PTH
kidney failure: lots of phosphate buidlup b/c can’t get rid of them
Mg2+ is absorbed where? Mg2+ excretion of affected by what?
Mg2+ is absorbed in the TAL and excretion affected by diuretics.
Parathyroid Hormone (PTH) ____ reabsorption of phosphate in the ____
Parathyroid Hormone (PTH) decreases reabsorption of phosphate in the proximal tubule
it inhibits the Na+/HPO4-/SO4- co transporter on the lumen side. This INCR excretion
when incr Ca2+ is released d/t bone breakdown, concentration HPO4 also incr so needs to be excreted
Parathyroid hormone (PTH) ____ calcium reabsorption in the ____
Parathyroid hormone (PTH) increases calcium reabsorption in the DT and CD
incr probabiity of “trippy channel”
Besides PTH, what else can incr calcium reabsoprtion in DT?
Vitamin D
Active form of Vitamin D is made where?
in the kidneys
How is Mg2+ is reabsorbed in the TAL and how is its excretion affected by diuretics?
- Normally: the lumen is neutral bc of Na+ and K+ and 2Cl- being transposrted into the cell (+2-2=0). The Ca2+ and Mg+ which travels paracellualary is not being reabsorbed bc there is no charge from the lumen (no electrical gradient) to drive the paracellular pathway
- With dieuretics: The loop dieuretic it incr reabsoprtion of Ca2+ and Mg+ because it inhibits the Na+K+2Cl- contransoprter. There is now a lot of Na+ and K+ sitting in the lumen in addition to the Ca2+ and Mg2+, so there is too many cations (too much positve charge)
- Ca2+ and Mg+ now is reabsorbed through paracelleur pathway because there is now an electral gradient.
