Vascular remodelling is well demonstrated in both human and experimental hypertension. Whether it develops in response to high blood pressure or as a marker of hypertension independently of any pressure level, it contributes in resistance arteries to maintaining an elevated blood pressure. Only recently, with the development of sensitive and reproducible methods, has remodelling of conduit arteries been assessed. A high resolution B-mode ultrasound technique can be used to measure arterial wall thickness and luminal dimension during the cardiac cycle. Changes in geometry and structure of conduit vessels have been observed in hypertensive patients or during experimental studies in animal models of hypertension. These changes may influence the buffering capacity of the conduit vessels, resulting in alteration of the dynamic component of the vascular impedance. Reduction of the systemic compliance may increase afterload and with time depress cardiac function. Ultrasonography apparatus is designed to measure local elastic properties and structural alterations and should be considered as such. Indeed, extrapolation of data acquired at a given arterial site to other parts of the vascular bed is hazardous. There exist other indirect methods based on pulse wave contour analysis and pulse wave velocity that can estimate global arterial compliance. Unfortunately, these methods have other limitations that restrict their use. Because conduit vessels represent one of the most important targets for pressure-induced lesions, namely atherosclerosis, they may be viewed as a surrogate endpoint in hypertension. Do we have evidence that vascular remodelling associated with hypertension predisposes to accelerated atherosclerosis? The purpose of this paper is to discuss the evidence that may support such a concept.