ds Flashcards
[Q:] How does EPI regulate plasma K+?
Increase EPI–> NaK ATPase–> decreases serum K+ by decreasing K+ reabsorption into extrarenal tissues and moveing it in the cell–> while increasing K+ excretion by the kidney.
[Q:] How does insulin regulate plasma K+?
High insulin–> + Na/K ATPase–> 3 Na+ out and 2 K+ inside the cell–> decrease plasma K+
[Q:] How does aldosterone regulate plasma K+?
Kidneys:
- aldosterone–> + K+ secretion–> + K+ excretion
Extrarenal tissues
- +aldosterone–> +K+ secretion–> goes into the intestinal fluids and saliva.
- Aldosterone also increases acid excretion via production of system alkalosis*
Receptors on afferent*** and efferent arteries –> vasoconstriction
alpha-1
Receptors on JG cells that, when stimulated, cause the release of renin–> + RAAS?
B1
Receptors on Na/K ATPase that when stimulated, result in
[increased Na+ reabsorption]?
alpha-1
- In alkalosis, K+ is exchanged for H+ ions in the cells (K+ enters the cells, H+ ions leave the cells) in order to try and balance H+ concentrations. Therefore, alkalosis can cause hypokalemia.
- Alpha-catecholamines decrease cell uptake by decreasing the activity of the Na/K ATPase, by reducing cAMP.
- When cells are damaged, potassium is free to be ejected into the plasma – causing hyperkalemia.
- Hyperosmolality enhances cell efflux due to a net increase in intracellular K concentration as a result of water leaving the intracellular fluid.
- Strenuous exercise directs potassium out of cells by an increasing alpha-catecholamines.
How to calculate filtered load
Filtered load=
[GFR] * [plasma concentration of x] * [% filterability]
*plasma proteins cannot be filtered. thus, anything bound to plasma proteins will not be filtered.
Characterstics of proximal tubule (4)
- Extensive brush border
- High SA
- Many mT to provide NRG for ATPases
- Where most reabsorption occurs.
PT has a proximal convoluted tubule (early) and a proximal straight tubule (late).
Most reabsorption occurs here and several anions and cations are secreted in the proximal tubule.
What allows the PT to undergo so much reabsorbtion and secretion?
Na/K ATPases on the BL membrane.
What role does Na+ play in K+ reabsorption in the proximal tubule?
In the PT, K+ reabsorption is similar to Na+ reabsorption.
- While Na+ reabsorption does not directly regulate K+, the amount of Na+ reabsorbed or excreted changes the environment of the nephron, INDRECTLY affecting K+
- Changing Na+ and Cl- reabsorption–> alter distal tubular flow and DT Na+ delivery –> later impacting K+
How is K+ reabsorbed in the PT?
-K+ reabsorption is driven by +TEPD that is created in the late PT-
What does a + TEPD mean?
What does a - TEPD mean?
+ TEPD–> build up of + charges
-TEPD–> build up of - charges
In order for us to be able to secrete K+, the Na/K+ ATPase requires Na+ to be reabsorbed in the distal tubule. How do we make sure enough Na+ arrives at the DT?
We must make sure that Na+ does not get reabsorbed too early. To do this, our goal is to increase the amount of K+ in the medulla.
K+ in the late DT and cortical CD
Because most of the K+ is reabsorbed in the PCT and the thick ascending limb, the late DT and cortical CD “fines tunes” the concentration of K+ through reabsorption and secretion.
K+ secretion in the late DT and cortical CD occurs via:
1. Principal cells
2. B-intercalated cells
K+ reabsorption in the late DT and cortical CD occur via what cells?
1. Type A-intercalated cells
What 3 factors stimulate K+ secretion?
- Increased ECF [K+]
- Aldosterone
- Increased tubular flow rate
What factors stimulate K+ reabsorption? (4)
1. K+ deficiency
2. Low K+ diet
3. Hypokalemia
4. K+ loss through severe diarrhea.
K+ secretion via principal cells
K+ secretion via B-intercalated cells
Type B-intercalated cells are active under alkalotic conditions.
- H+ concentration in the ISF is low.
- Inside is the type B-intercalated cell, [CO2+H20–> HCO3- + H+], causing a build up of HCO3 and H+.
- HCO3-/Cl- exchanger on the apical membrane secetes HCO3- into the urine and reabsorbs Cl-.
- H/K ATPase on the BL membrane moves K+ into the cell and reabsorbed H+ into the ISF.
- K+ is then secreted via K+leak channels
K+ reabsorption via Type A-intercalated cells
Type A-intercalated cells are active under acidic conditions. They helps us secrete H+ ions and reabsorb HCO3.
- In the ISF, H+ concentrations are high.
- [H+ + HCO3- → CO2]
- [CO2 then moves inside the intercalated type-A cells]
- Inside, we reconvert [CO2+ H20]–> [HCO3 and H+ ions]
- H+ ions increase and are secreted via the H/K+ ATPases on the apical membrane which allow H+ to exit and K+ to be reabsorbed into the cell.
- As K+ increases in the cell, it is reabsorbed into the ISF via K+ leak channels that are located on the apical membrane.
- *HCO3- inside of the cell will be reabsorbed back into the ISF via HCO3-/Cl- exchanger.
The most important factors the encourage K+ secretion when it builds up in the ECF are (5)
- Increase NaK ATPase pumps on the BL membrane of principals cells.
- Increase synthesis and insertion K+ channels on the apical membrane
- Increase in aldosterone
- Increase distal tubule flow rate (increase Na+ delivery to the DT to promote K+ secretion)
- Reduced back leakage of K+ from ICF–> renal interstituim (less K+ leaves from ICF through the BL membrane, causing more to make it out of the apical membrane to be secreted)
What exactly do we mean by “flow rate”?
Increased flow rate does what?
- Increased flow rate–> dilutes K+ secreted into the lumen–> increasing K+ concentration gradient between the ICF and tubular fluid–> enhances K+ secretion.
- Increased flow rate also increases Na+ delivered to the distal tubule for reabsorption–> Na+ reabsorbed via ENaC channels–> causing K+ to be secreted.
What exactly do we mean by “flow rate”?
Decreased flow rate does what?
- Decreased flow rate –> K+ concentration build up early in the tubule–> decreasing concentration gradient between tubular fluid and cell (ECF and ICF)–> slows K+ secretion
What happens when we have a high Na+ diet (eat something REALLY salty)?
What happens when we have a high K+ diet (eat several bananas)?
High K+ diet–>
Insulin will move K+ into the princpal cells–>
Build up of K+ in the cell will increase the concentration gradient–>
–> K+ will be secreted from the PC–> urine
This is why we don’t become hyper/hypokalemic during times of increased or decreased salt intake.
Why is the relationship between the distal tubule flow rate and K+ secretion important?
It helps aldosterone to [regulate K+] and [Na+ excretion]
What is the difference between alkalosis and alkalemia?
- Alkalosis–> high pH (low H+ ions) in the ECF.
- Alkalemia–> physiologically high blood pH.
Alkalosis is typically a problem with hypokalemia.
How does this occur?
mneumonic: alkalosis; k is lo
Alkalosis is typically a problem with hypokalemia.
Alkalosis: + activity of Na/K+ ATPase pump (and adds K+ channels into apical membrane) –> increases intracellular K+ concentration–> K+ passively moves from the cell to the lumen–> K+ is secreted
- Result: HYPOKALEMIA
What is the difference between acidosis and acidemia?
- Acidosis–> increase in H+ ions in the ECF
- Acidemia–> physiologically low blood pH
Acidosis typically a problem with hyperkalemia.
How does this occur?
Acidosis: decreases the activity of the Na/K ATPase (and decreases K+ channels on the apical membrane) –> K+ does not move into cell–> decrease in intrallular K+ concentration–> decrease diffusion of K+ into the lumen–> decreases K+ secretion
- RESULT: Hyperkalemia
RECAP:
Alkalosis is association with _____kalemia, _____ K+ secretion
Acidosis is associated with _____kalemia, ____K+ secretion
Alkalosis is association with hypokalemia, increasing K+ secretion.
Acidosis is associated with hyperkalemia, decreasing K+ secretion.
Chronic acidosis ______K+ secretion.
stimulate
When problems are chronic, our body learns to compensate for these dillemmas. Chronic inhibition of the Na/K ATPase will prevent us from reabsorbing solutes and fluid, which will increase our tubular flow rate.
- As a result, more Na+ is delivered to the distal tubule, which will increase K+ secretion.
- Also, we will activate the RAAS system–> aldosterone–> K+ secretion
How does increased Na+Cl- reabsorption upstream affect Na+ delivery to CNT and CCD and subsequent events?
[Decrease Na+ delivery to CNT and CCD] –> [decrease lumen-negative potential difference] –> [decrease K+ secretion]
Aldosterone is a kaliuretic hormone, induced by hyperkalemia.
However, until certain condition assx with marked induction of aldosternoe, such as dietary Na+ restriction, Na+ balance is maintained without ________.
Effecting K+ (aldosterone paradox)
Diuretics that inhibit Na+ reabsorption–>
promote K+, except for K+ sparing drugs.
Low K+ diet
Low K+ diet–> princpal cells are depleted of K
- Intracellular concentration of K+ decreases–> decreases the driving force for K+ secretion
- Alpha-intercalated cells will reabsorb K+
RESULT: LOW RATES OF K+ excretion
DISTAL TUBULAR FLOW RATE WILL COMPENSATION FOR
changes in aldosterone, which affects K+ secretion and absorption
What happens in cases of acidosis
- Na/K ATPase pumps will be inhibited
- Decrease in intracellular K+
- K+ will not be secreted
to compensate
- Decrease proximal tubule reabsorption
- Increase distal tubular flow rate
- Increase Na in the DT
4 . increase K secretion
What happens in cases of volume expansion
Volume expansion: increase in NaCl
- Decrease in aldosterone
- Decrease K secretion
to compensation;
- Decrease proximal tubule reabsorption
- Increase distal tubular flow rate
- Increase Na in the DT
4 . increase K secretion
What happens in cases of high water intake
- Decrease ADH
- Decrease distal K+ secretion and decrease distal water absorption
- Increase distal flow
- increase distak K secretion
What happens in vases of volume contraction
- Decreased ECF—> decreased NaCl
- Renin
- ANG II
- Increase aldosterone
–> increase K+ secretion
to compensate;
- Decrease GFR
- Decrease distal flow
- decrease K+ secretion
