Many factors that inhibit receptor-mediated endocytosis (RME) at postreceptor level in vitro have been described: (i) high concentration of urea, (ii) lowering of intracellular pH, (iii) hypotonic or hypertonic media, (iv) intracellular potassium depletion, (v) depletion of cellular ATP, (vi) inhibition of the enzyme transglutaminase, (vii) impairment of receptor recycling by rising of the endosomal pH, (viii) disruption of microtubules. Nearly all or all of the factors mentioned above are present as disturbances of homeostasis in uremia. The magnitude of the factors inhibiting RME in vitro is considerably greater than the deviations observed in uremia, but in vitro almost complete inhibition of RME is aimed and also in uremia all of the factors act together. The hypothesis that RME is inhibited in uremia is supported by the metabolism of macromolecules known or supposed to be internalized by this process. Although glucose intolerance in uremia is due to a postreceptor defect in insulin action, impaired RME at postreceptor level, to the best of my knowledge, has not been pointed as a general feature of uremia. In addition to uremia, there might be other clinical examples of inhibited RME at postreceptor level as well.
Biomedical Reviews 1993; 2: 57-75.
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