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  1. Abstract We propose a relatively simple two-dimensional mathematical model for maladaptive inward remodeling of resistive arteries in hypertension in terms of vascular solid mechanics. The main premises are: (i) maladaptive inward remodeling manifests as a reduced increase in the arterial mass compared to the case of adaptive remodeling under equivalent hypertensive pressures and (ii) the pressure-induced circumferential stress in the arterial wall is restored to its basal target value as happens in the case of adaptive remodeling. The rationale for these assumptions is the experimental findings that elevated tone in association with sustained hypertensive pressure down-regulate the normal differentiation of vascular smooth muscle cells from contractile to synthetic phenotype and the data for the calculated hoop stress before and after completion of remodeling. Results from illustrative simulations show that as the hypertensive pressure increases, remodeling causes a nonmonotonic variation of arterial mass, a decrease in inner arterial diameter, and an increase in wall thickness. These findings and the model prediction that inward eutrophic remodeling is preceded by inward hypertrophic remodeling are supported by published observations. Limitations and perspectives for refining the mathematical model are discussed. 
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  2. Abstract We propose a novel structure-based two-dimensional (2D) mathematical model of hypertension-induced arterial remodeling. The model is built in the framework of the constrained mixture theory and global growth approach, utilizing a recently proposed structure-based constitutive model of arterial tissue that accounts for the individual natural configurations of and stress interaction between elastin and collagen. The basic novel predictive result is that provided remodeling causes a change in the elastin/collagen mass fraction ratio, it leads to a structural reorganization of collagen that manifests as an altered fiber undulation and a change in direction of the helically oriented fibers in the tissue natural state. Results obtained from the illustrative simulations for a porcine renal artery show that when remodeling is complete the collagen reorganization might have significant effects on the initial arterial geometry and mechanical properties of the arterial tissue. The proposed model has potential to describe and advance mechanistic understanding of adaptive arterial remodeling, promote the continual refinement of mathematical models of arterial remodeling, and provide motivation for new avenues of experimental investigation. 
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