K5 - Identification of Shear Stress as a Potential Vasoconduction Signal Across Microvascular Networks

Introduction: : Shear stress generated by microvascular blood flow plays a central role in initiating ion-mediated signaling and regulating microcirculatory dynamics. This mechanical cue is recognized for its ability to induce localized vasomotion, yet its broader role as a vasoconduction signal remains poorly defined. Specifically, the extent to which shear stress changes propagate through microvascular networks following localized vasoconstriction is not well characterized. Understanding this could reshape how we view systemic regulation of tissue perfusion. In this study, we investigate whether localized vasoconstriction can produce physiologically meaningful changes in shear stress across entire microvascular networks and determine how these changes are spatially distributed. The goal is to uncover fundamental insight into the hydrodynamic behavior of shear stress as a signaling mechanism in vascular biology.

Materials and

Methods: : We used high-resolution images of mesenteric microvascular networks extracted from adult rat tissues. These networks were reconstructed into computational models and integrated with a segmental blood flow simulation framework to examine hemodynamic changes under various vasoconstriction scenarios1. Simulated constrictions were applied at different vessel types, including arterioles and capillaries, and an additional network from muscle tissue was analyzed for comparison. Shear stress values were computed under baseline and constricted states. Changes in shear stress were then spatially mapped across the networks to assess propagation patterns and magnitude. The model captures microvascular network geometry, topology, and vessel-specific hemodynamic parameters to mimic realistic physiological conditions, ensuring that predicted shear stress changes reflect biologically relevant scenarios.

Results, Conclusions, and Discussions:: Simulation results show that vessel-specific vasoconstriction can produce substantial and heterogeneous changes in wall shear stress throughout microvascular networks. Arteriolar constriction scenarios resulted in elevated shear stress levels, often exceeding 30 dyne/cm², not only near the site of constriction but also at remote locations, several millimeters away. Capillary constriction caused more localized changes, but still influenced shear stress patterns downstream. These effects were consistent across different network types, including a muscle microvascular network. Importantly, the magnitude and spatial extent of shear stress propagation depended on local network architecture and capillary density. Regions with dense capillary beds exhibited different propagation patterns than sparse ones, suggesting that vascular topology significantly affects how mechanical signals travel within the network. These findings support the idea that shear stress, beyond its role in local vasomotion, may act as a long-range hydrodynamic signal contributing to vasoconduction. This has implications for how microcirculatory blood flow is coordinated and regulated across tissues, especially under dynamic physiological or pathological conditions. In conclusion, this study strengthens the hypothesis that shear stress is a key hydrodynamic signal in microvascular function and vasoconduction. The physiological relevance and spatial distribution of predicted shear stress changes point toward a more integrative understanding of how local mechanical stimuli may influence systemic microvascular behavior. This study motivates future work exploring time-dependent interactions between shear stress and electrical signaling to better understand microvascular flow coordination.

Acknowledgements and/or References (Optional):: 1 Sweat, Stapor, and Murfee, LYMPHAT RES BIOL., 2012.
National Science Foundation grant CBET 2309559, and National Institutes of Health grant R21HL159501.