Mammalian cells of various types exhibit the remarkable ability to adapt to externally-applied mechanical stresses and strains. Because of this adaptation, cells can maintain their endogenous mechanical tension at a preferred (homeostatic) level, which is essential for normal physiological functions of cells and tissues and provides protection against various diseases, including atherosclerosis and cancer. Conventional wisdom is that the cell possesses the ability to maintain tensional homeostasis on its own. Recent findings showed, however, that isolated cells cannot maintain tensional homeostasis. Here we studied the effect of multicellular interactions on tensional homeostasis by measuring traction forces in isolated bovine aortic endothelial cells and in confluent and non-confluent cell clusters of different sizes. We found that in isolated cells the traction field exhibited a highly dynamic and erratic behavior. However, in cell clusters, dynamic fluctuations of the traction field became attenuated with increasing cluster size at a rate which was faster in non-confluent than in confluent clusters. The driving mechanism of attenuation of traction field fluctuations was statistical averaging of the noise and the impeding mechanism was non-uniform stress distribution in the clusters, which resulted from intercellular force transmission known as a "global tug-of-war". These results showed that isolated cells could not maintain tensional homeostasis, which confirmed previous findings, and that tensional homeostasis is a multicellular phenomenon, which was a novel finding.