Chapter 29: Renal Regulation of K+, Ca++, Na+/Fluid Volume (Discussion 3) Flashcards
Location of K+ in the body
Primarily in cells (4.2 mEq/L ECF vs. 140 mEq/L ICF) High ECF [K+] can cause cardiac arrhythmias/death
Hypokalemia
Low plasma [K+]
Hyperkalemia
High plasma [K+]
Factors that shift K+ into cell
Aldosterone (excess = Conn’s syndrome) Insulin B-adrenergic stimulation Alkalosis
Factors that shift K+ out of cell
Deficient Aldosterone (Addison’s disease) Diabetes mellitus B-adrenergic blockade Acidosis (H+ inhibits Na-K pump) Cell lysis Strenuous exercise ↑ECF osmolarity
Excretion/Renal Regulation of K+
65% reabsorbed in proximal tubule
25-30% reabsorbed in loop of Henle (relatively constant; Na/2Cl/K pump action in thick ascending limb)
Reabsorb (minimally) by intercalated cells (H/K ATPase)
Secrete by principal cells (diffusion)
Factors that control excretion/renal regulation of K+
- ECF [K+]: Increase in ECF concentration will:
- Stimulate Na-K pump
- Reduce back-leakage
- Stimulate aldosterone
- Aldosterone: Increase in aldosterone will:
- Stimulate Na-K pump
- Increase in the # of luminal K+ channels
- Tubular flow rate: increase in flow rate
- “Washdown” of K+ –> Increase in diffusion
Location of Ca++ in the body
- Higher concentrations in ECF but much lower quantities than Na+
- Most ECF Calcium bound to plasma proteins/non-ionized –> 2.4 mEq/L active Ca++
- Binding affected by pH (acidosis –> decreased binding)
- Only free Ca++ filtered into nephron (~50%)
- 99% reabsorbed (~65% at proximal tubule)
- ~99% stored in bone (acts as Ca reservoir)
Hypocalcemia
Decrease [Ca++] ECF
Cause nerve/muscle hyperexcitability –> tetany
Hypercalcemia
Increase [Ca++] ECF
Depress neuromuscular excitability –> arrhythmias
Parathyroid Hormone (PTH)
Stimulated by low ECF [Ca++] or high [PO43-]
Regulate [Ca++]
- Increase bone resorption (release Ca++)
- Increase reabsorption of Ca++ in kidneys (acts at thick ascending loop/distal tubule)
- Activate vitamin D –> increase intestinal reabsorption of Ca++
Regulate PO43-
- Increase bone resorption (release PO43-)
- Decrease PO43- reabsorption in renal tubules
Na+/Volume Regulation
Major regulator is pressure natriuresis & diuresis (more powerful in chronic hypertension)
- slight increase in GFR
- High peritubular capillary hydrostatic pressure –> decrease reabsorption of Na/H2O
- High arterial pressure –> decrease angiotensin II/aldosterone formation –> decrease reabsorption of Na/H2O
Sympathetic Nervous Control of Excretion
Baroreceptors sense low BP –> sympathetic stimulation
–> constrict renal arterioles –> decrease GFR –> increase reabsorption of water/salts –> increase renin/angiotensin II/aldosterone –> increase tubular reabsorption
Angiotensin II
Increase NaCl/H2O reabsorption
Amplify pressure natri/diuresis (thus important for controlling NaCl/H2O reabsorption)
ACE inhibitors/angiotensin II receptor antagonists block its effects and shift excretion curve to lower pressures
Aldosterone
Increase Na+/H2O reabsorption and K+ secretion
During over-secretion of aldosterone, rise in BP will be minimized by pressure natriuresis