TY - JOUR

T1 - A mechanism for arteriolar remodeling based on maintenance of smooth muscle cell activation.

AU - Jacobsen, Jens Christian Brings

AU - Mulvany, Michael John

AU - Holstein-Rathlou, N.-H.

N1 - Keywords: Adaptation, Physiological; Animals; Arterioles; Blood Pressure; Computer Simulation; Elasticity; Humans; Hypertension; Models, Cardiovascular; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Rats; Stress, Mechanical; Time Factors; Vasoconstriction; Vasodilation

PY - 2008

Y1 - 2008

N2 - Structural adaptation in arterioles is part of normal vascular physiology but is also seen in disease states such as hypertension. Smooth muscle cell (SMC) activation has been shown to be central to microvascular remodeling. We hypothesize that, in a remodeling process driven by SMC activation, stress sensitivity of the vascular wall is a key element in the process of achieving a stable vascular structure. We address whether the adaptive changes in arterioles under different conditions can arise through a common mechanism: remodeling in a stress-sensitive wall driven by a shift in SMC activation. We present a simple dynamic model and show that structural remodeling of the vessel radius by rearrangement of the wall material around a lumen of a different diameter and driven by differences in SMC activation can lead to vascular structures similar to those observed experimentally under various conditions. The change in structure simultaneously leads to uniform levels of circumferential wall stress and wall strain, despite differences in transmural pressure. A simulated vasoconstriction caused by increased SMC activation leads to inward remodeling, whereas outward remodeling follows relaxation of the vascular wall. The results are independent of the specific myogenic properties of the vessel. The simulated results are robust in the face of parameter changes and, hence, may be generalized to vessels from different vascular beds.

AB - Structural adaptation in arterioles is part of normal vascular physiology but is also seen in disease states such as hypertension. Smooth muscle cell (SMC) activation has been shown to be central to microvascular remodeling. We hypothesize that, in a remodeling process driven by SMC activation, stress sensitivity of the vascular wall is a key element in the process of achieving a stable vascular structure. We address whether the adaptive changes in arterioles under different conditions can arise through a common mechanism: remodeling in a stress-sensitive wall driven by a shift in SMC activation. We present a simple dynamic model and show that structural remodeling of the vessel radius by rearrangement of the wall material around a lumen of a different diameter and driven by differences in SMC activation can lead to vascular structures similar to those observed experimentally under various conditions. The change in structure simultaneously leads to uniform levels of circumferential wall stress and wall strain, despite differences in transmural pressure. A simulated vasoconstriction caused by increased SMC activation leads to inward remodeling, whereas outward remodeling follows relaxation of the vascular wall. The results are independent of the specific myogenic properties of the vessel. The simulated results are robust in the face of parameter changes and, hence, may be generalized to vessels from different vascular beds.

U2 - 10.1152/ajpregu.00407.2007

DO - 10.1152/ajpregu.00407.2007

M3 - Journal article

C2 - 18184768

VL - 294

SP - R1379-89

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 4

ER -