Modulation of intracellular potassium and ATP: Effects on coated pit function in fibroblasts and hepatocytes

Abstract

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 4μm 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 > 95% by metabolic inhibitors, receptor‐mediated endocytosis is unaffected.