This dissertation studies how hydrodynamic forces are transmitted across the membranes of endothelial cells and bone cells (osteocytes) via extracellular matrices. Firstly, I apply large deformation theory for ‘elastica’ to describe the restoration of the core protein fibers in the endothelial glycocalyx (EG) after being matted by the passage of a white blood cell. By matching the predicted time-dependent thickness of the EG with experiments I obtain an estimate of 490 pN•nm² for the flexural rigidity of the core protein fibers. Thus, the EG is sufficiently stiff to function as a mechanotransducer. The core proteins are also barely deflected by the physiological motion of red blood cells (RBCs). In contrast, arrested RBCs crush the EG and the viscous draining resistance of the EG layer is essential for preventing adhesive intercellular interactions between endothelial cells and RBCs. Secondly, I model the response of the EG to steady or oscillating shear applied at its edge, and extend this analysis to apply to the microvilli and cilia on kidney cells. In the case of oscillating shear, I find that the motions of both the fluid and structural elements, including the EG and microvilli and cilia on kidney cells, are in a quasi-steady state at physiological conditions. Thirdly, I develop a realistic 3-D structural model for the core actin bundle in osteocytic processes, and greatly refine the strain amplification model for bone mechanotransduction proposed by You et al. (2001, J. Biomech. 34:​ 1375). The new model predicts a cell process that is 3 times stiffer than You et al. (2001), but hoop strains > 0.5 percent for tissue level strains > 1000 μ strain at 1 Hz and > 250 μ strain at frequencies > 10 Hz. This strain amplification model provides a more likely hypothesis for the excitation of osteocytes than the fluid shear hypothesis previously proposed in Weinbaum et al. (1994, J. Biomech. 27:​ 339). Finally, I study the fluorescence uptake by osteocyte-like MLO-Y4 cells incubated with agonists and antagonists to purinergic P2X₇ receptors. The results suggest the involvement of P2X₇ receptors in the signaling pathway for the mechanotransduction of osteocytes.