A potential role of smooth muscle tone in early hypertension: a theoretical study

A conspicuous long-term consequence of hypertension is a thickening of the arterial wall, which many suggest returns the circumferential wall stress toward its normal value. This thickening results from an increase in smooth muscle and extracellular matrix, with the associated growth and remodeling processes depending on a host of regulatory signals that likely include the altered mechanical environment. Although the precise mechanotransduction pathways remain unknown, we propose that vasoconstriction may be an early response of the arterial wall to a step-change in pressure. In particular, computations suggest that such a response can decrease the magnitude and transmural gradients of the pressure-induced wall stresses and return the mean wall shear stress toward its homeostatic value. Such an initial 'compensatory vasoconstriction' could also help set into motion subsequent growth and remodeling responses due to growth regulatory characteristics of the vasoactive molecules (e.g., nitric oxide, endothelin-1, angiotensin-II). Although the consequences of growth and remodeling have been the focus of prior biomechanical and histological studies, early responses dictate subsequent developments and therefore deserve increased attention in vascular biomechanics and mechanobiology.