The mechanisms for stress-induced changes in hematocrit and blood viscosity are unclear. Twenty-two males completed experimental (30 min baseline, 10 min mental stress, 30 min recovery) and no-stress control conditions (70 min). Hemostatic and hemodynamic activity were measured throughout. Hematocrit, colloid osmotic pressure, and blood viscosity displayed parallel patterns: a progressive increase with stress, followed by a gradual recovery. Correlational and covariance analyses indicated that the increase in hematocrit may be mediated by arterial pressure whereas recovery may be mediated by colloid osmotic pressure. Analyses also indicated that acute changes in blood viscosity may depend on hematocrit. These data suggest that stress disturbs hematocrit, colloid osmotic pressure, and blood viscosity through arterial pressure. Poststress, elevated colloid osmotic pressure may drive its own recovery and that of hematocrit and blood viscosity.