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