PURPOSE: To examine changes in retinal perfusion density (PD) following short-term exposure to optically induced myopic defocus, an ocular growth-inhibitory stimulus, and achromatic digitally simulated myopic blur, an ocular growth stimulus. METHODS: The left eyes of 12 emmetropic and 12 myopic healthy young adults (mean ± SEM age: 24 ± 1 years) underwent optical coherence tomography angiography to assess retinal PD before and following 60 minutes of blur exposure. Optical myopic defocus was induced by viewing a video through +2 D lenses, digitally simulated myopic blur by viewing the same video filmed with a +2 D defocused camera, and the control (no-blur) condition by viewing the original video through optimal refractive correction. PD changes were examined using linear mixed models, with the control-condition changes as a covariate. RESULTS: A significant blur by eccentricity interaction was observed (P < 0.001), with the overall retinal PD increasing with optical myopic defocus compared to simulated myopic blur in the fovea by 2.9% ± 1.0% (P = 0.003) but decreasing in the outermost 2- to 3-mm parafovea by -2.3% ± 0.5% (P < 0.001). Significant PD changes were also observed associated with the blur condition, perfusion layer, eccentricity, and refractive status (interaction, P = 0.04). The most pronounced effects were observed in the foveal deep capillary plexus, where emmetropes exhibited increased PD during optical myopic defocus and decreased PD during simulated myopic blur (3.8% ± 2.3% vs. -6.4 ± 2.2%; P < 0.001), but myopes exhibited significantly different responses compared with emmetropes to both the optical blur (-4.0% ± 2.3%; P = 0.035) and the simulated myopic blur (0.7% ± 2.3%; P = 0.046). CONCLUSIONS: Significant blur-driven changes were observed in the retinal PD of emmetropic eyes, increasing with optical myopic defocus but decreasing with simulated myopic blur of comparable magnitude, particularly in the foveal deep capillary plexus, with these responses not observed in myopic eyes. These bidirectional retinal perfusion responses are unlikely to be driven solely by blur magnitude or contrast modulations and are more plausibly related to vergence cues that were present with optical myopic defocus but absent in digitally simulated myopic blur.