Physiology

1. Dr Alexander M. Tungu (MD, PhD, MBA-CM
Cand.)
Department of Physiology

2.  Normal ECF conc. = 3.5 - 5.2 mEq/L
 NOTE: Similar to H+, Potassium concentration is also
carefully controlled in body fluids

3.  Electrophysiologic:
K+ major determinant of the resting potentials and excitability of
muscles and neurones
K+ disturbances cause conduction dysfunction
 Epithelial transport:
Cell solute uptake and elimination depends on electrical and chemical
gradients set up by the Na+/K+ ATPase
 Cell volume regulation, chemical reactions etc

4.  Over 98% of K is in ICF
(Other ions mostly within cells are Mg and
Phosphate)
 Since both plant and animal cells
contain K, K intake is a constant
feature of the diet
 Steady state:
K Intake=K excretion
(minimum/obligatory K+ loss = 10mEq/day)

5.  Internal balance of K concerns itself with the distribution of K
between the intracellular and extracellular space
 Regulates/buffers acute changes in K concentration
 External K balance concerns itself with the matching of K
intake and renal excretion, while maintaining normal
extracellular and intracellular Concentrations
 The renal regulation of K excretion is the result of K
secretion in the distal tubule and collecting duct

6.  Internal balance:
Catecholamines, Insulin, pH, Osmolarity, cell lysis, exercise,
anabolism.
 External balance:
Oral intake and renal excretion (role of Aldosterone)

7.  Insulin:
Stimulated by a meal
K+ enter cells by increasing Na-K-ATPase.
Diabetics may have high K+
Treatment of hyperkalemia may include insulin and glucose
 Catecholamines:
Beta-2 agonists stimulate K+ uptake into cells by increasing Na-K-ATPase
Beta agonists (eg; Salbutamol) may cause hypokalemia, and stress can lower
the serum potassium
People taking beta blockers (eg; Propranolol) may have a tendency to have
high serum potassium

9.  Acid-base: There is an apparent inverse relationship
between serum [K+] and blood pH
 That is, H+ movement into the cell is counterbalanced by K+
efflux (and vice-versa) to maintain electrical neutrality
 An example; in inorganic metabolic acidosis, pH falls and
serum [K+] rises.

13.  90% of the K+ transported by
NKCC is recycled via K+
channels (ROMK),resulting in
minimal net K+ reabsorption by
the TAL (~ 25% of filtered K+)

14. Most K+ has been reabsorbed before the CD.
The usual state is the need to excrete K+
The CD principal cells are the regulatory sites mediating K+
secretion.
In K+ deficient state:
The CD intercalated cells will continue to reabsorb
potassium

21.  Hyperkalemia: [K ] > 6 mEq/l.
Can elicit decreased excitability of neurons and muscle, muscle paralysis,
cardiac arrhythmias and metabolic acidosis (due to H+ efflux from cells
and reduced renal NH3 generation)
 Hypokalemia: [K ] < 3 mEq/l.
Can elicit mental confusion, muscle weakness, decreased excitability of
neurons, reduced ability to concentrate urine (nephrogenic diabetes
insipidus) and metabolic alkalosis (due to H+ influx and increased NH3+
gen)

23.  Results from resistance to the action
of ADH
 Reduced ability to concentrate urine
(nephrogenic DI)
 Low K+ in serum and filtrate
 May reflect;
Resistance of ADH at the site of action (V2
receptors in the collecting duct)
Impaired NKCC activity in TAL
Impaired Countercurrent multiplication

25.  Most diuretics acting before the
Collecting duct (Carbonic anhydrase
inhibitors, Osmotic, Loop, Thiazides)
tend to increase distal flow and
stimulate potassium excretion,
leading to hypokalemia.
 However, diuretics that act on the
collecting duct itself (ACE-inhibitors,
Potassium sparing diuretics) inhibit
K+ secretion, leading to K+ retention
and risk of hyperkalemia

26.  Internal and External K+ balance
 Role of the kidneys in External K+ balance
 Factors influencing Internal/External K+ balance
 Disorders of Potassium metabolism
 Impact of Diuretics on Potassium balance