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
