L8 Reg Of K And Multivalent Ions Flashcards
Regulation of potassium: importance
Role of K in the excitability of nerve and muscle
Resting membrane potential depends on K conc gradient
ECF K is a function of two variable
Amount of K in the body (input=output)
Distribution of K between ICF and ECF
Regulation of internal K distribution
Most inside cells ~98%
Changes in conc are readily detected
Under physiological control via 3 hormones:
Epinephrine
Insulin
Aldosterone
Epinephrine in controlling K
Alpha 1 receptor activation causes a shift of K out of cells and may results in hyperkalemia (K increases in ECF)
Beta 2 receptor activation stimulates K uptake into cells and may cause hypokalemia (low K in ECF). B2 antagonists block this action and can cause hyperkalemia
Beta 2 thought to be more dominant receptor, more likely observed
Insulin in controlling K distribution
Increases K uptake into cells (hypokalemic)
Responsible for dietary uptake of K into cells after a meal
Stimulates Na-KATPase
Body wide effects
Aldosterone in controlling K distribution
Increase K uptake into tubule cells and increase K excretion
Stimulates Na-KATPase
Other factors in regulation of internal K distribution
Hyper osmolarity
Exercise
Acid-base
Acidosis- movement of K out of cells
Alkalosis- movement of K into cells
Generalizations for K
Input=output for balance to occur
Dietary K is variable (50-150mEq/day)
Transport in the PT and LOH does not change in the face of increases of decreases total body K
Physiological regulation of K in the distal tubule and CD
K secretion also increases when
Na load to distal nephron increases
Increased Na load to principal cells stimulates Na-KATPase which increases intracellular K conc s
Loop diuretics, thiazides, kaliuresis
Increased delivery Na to distal nephron will increase K loss
Increased Na entry via apical Chanel stimulates Na-KATPase
This increase the intracellular K conc and K secretion
Amiloride and spironolactone do not have this effect, they are referred to as potassium-sparing
Effect of a high K diet - aldosterone
Aldosterone stimulated by high plasma K
Promotes K secretion By
Stimulation of basolateral membrane Na-KATPase
Increasing luminal membrane perm to K
Occurs in principal cells
Apical K channel up-regulated in addition to Na-KATPase
Lumenal potential -50mV - electrochemical gradient strongly favors K secretion
Effect of low K diet
Homeostatic response: decrease K excretion
PT and LOH reabsorb 87% of the filtered K
Remaining K reabsorbed in distal nephron
K reabsorption mechanism
Occurs in alpha intercalated cells of distal nephron
K reabsorption in exchange for H secretion
K diffuses across basolateral membrane
Regulation of Ca
Major roles: Bone formation Cell division and growth Blood coagulation Hormone response coupling Excitation contraction coupling
Stores:
99% in bone
1% in ICF
0.1% in ECF
Normal plasma Ca
2.5mM can exist in 3 forms
50% ionized Ca2+ biologically active
10% complexed to anions (CaPO4)
40% bound to plasma proteins (can’t be filtered)
Renal handling of Ca
Ca is filtered and reabsorbed
60% of plasma Ca is filtered
FL =(GFR)(Pca)(0.6)
Reabsorption occurs throughout the nephron (99%) except descending limb of LOH
Only 1% of filtered Ca appears in urine
Renal homeostatic mechanisms operate by altering the rate of reabsorption
Ca reabsorption by proximal tubule
Passive reabsorption
Coupled to Na- factors that affect Na reabsorption also affect Ca. When Na uptake is high, so is Ca uptake
Reabsorbed through paracellular route
Thick ascending limb of LOH
Lumen positive potential drives Ca reabsorption
Some K transported by NKCC2 diffuses back into lumen
Lumen becomes slightly pos (+7mV)
Ca Enters paracellular pathway
Loop diuretics interfere with Ca reabsorption ( they’re used to treat hypercalcemia)
Calcium and the distal tubule
Across apical membrane via Ca channels
Across basolateral membrane in 2 ways
Active transport via Ca-ATPasr
Na-Ca exchange
PTH stimulates Ca uptake in DT
Mediated by cAMP
Thiazide diuretics increase Ca reabsorption
Thiazides inhibit NaCl reabsorption but stimulate Ca reabsorption
Thiazides decrease Na inside which increase inward movement of Na via Na/Ca exchanger
Increases Ca reabsorption from luminal fluid
