Smooth muscle cell function and organization of the resistance artery wall

Remodeling of the vascular wall occurs in several cardiovascular pathologies. A structural change in diameter necessarily involves reorganization in both cellular and extracellular matrix components. The significance of matrix remodeling in vascular pathologies is well appreciated, while plasticity of vascular smooth muscle cells (SMC) received less attention. Such contractile plasticity is defined as a change of the diameter-dependent capacity for active force generation.
The aim of this thesis is to investigate how small arteries maintain their stability and functionality, from a biomechanical perspective, during physiological and pathological remodeling. We propose that vascular SMC plasticity is an important process in inward remodeling of small arteries.
The most important findings were; the contractile properties of SMCs in resistance vessels are subject to rapid changes. Such contractile plasticity is influenced by externally imposed vasoconstriction and strain. Vasoconstrictors and specifically ET-1 induced inward SMC plasticity in small arteries while chronic strain results a shift of tension generating capacity to larger diameters. This process may maintain optimal matching of SMC and matrix biomechanics during growth and remodeling. The work contributes to a better understanding of vascular wall biomechanics and adaptation, and may lead to new options for diagnosis and treatment of cardiovascular diseases.