We have previously shown that endothelin‐1 increases glucose uptake in astrocytes. In the present work we investigate the mechanism through which endothelin‐1 (ET‐1) increases glucose uptake. Our results show that ET‐1 activates a short‐term and a long‐term mechanism. Thus, ET‐1 induced a rapid change in the localization of both GLUT‐1 and type I hexokinase. These changes are probably aimed at rapidly increasing the entry and phosphorylation of glucose. In addition, ET‐1 upregulated GLUT‐1 and type I hexokinase and induced the expression of isoforms not normally expressed in astrocytes, such as GLUT‐3 and type II hexokinase. These changes provide astrocytes with the machinery required to sustain a high rate of glucose uptake for a longer period of time. Our previous work had suggested that the effect of ET‐1 on glucose uptake was associated with the inhibition of gap junctions. In this work, we compare the effect of ET‐1 with that of carbenoxolone, a classical inhibitor of gap junction communication. Carbenoxolone increased glucose uptake to the same extent as ET‐1 following the same mechanisms. Thus, carbenoxolone induced a rapid change in the localization of both GLUT‐1 and type I hexokinase, upregulated GLUT‐1 and type I hexokinase and induced the expression of GLUT‐3 and type II hexokinase. When the inhibition of gap junction was prevented by tolbutamide, neither ET‐1 nor carbenoxolone were able to increase the levels of GLUT‐1, GLUT‐3, type I hexokinase or type II hexokinase, indicating that these events are closely related to gap junctions.