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Previously we reported that cultured human fibroblasts depleted of intracellular potassium (K+) had a reduced number of surface coated pits and were unable to internalize receptor-bound molecules such as low density lipoprotein (LDL). We have extended these studies in two important ways. First, we have developed a method for modulating the number of coated pits in situ. Human fibroblasts incubated in K+-free buffer that contains 4 micron nigericin rapidly become depleted of K+ and lose the ability to internalize 125I-LDL. When rat livers are perfused with the same buffer, there is a 75% decrease in the number of surface coated pits in hepatocytes. Secondly, we have explored the possibility that K+-depletion effects coated pit function by lowering intracellular ATP. We found that although this protocol lowers intracellular ATP by 40-70%, when ATP concentrations are lowered greater than 95% by metabolic inhibitors, receptor-mediated endocytosis is unaffected.
Larkin et al. (Sun,) studied this question.