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For a given cardiac function, the cyclic blood pressure (BP) curve results from 2 different phenotypes: the mean arterial pressure (MAP), a steady component reflecting the resistance of the microvascular network, and pulse pressure (PP), another component corresponding to large artery stiffness and wave reflections. Around birth, cardiovascular (CV) survival is critically influenced by the coupling between the heart and thoracic aorta, and hence, the adequacy of the Windkessel function, the magnitude of aortic elastin accumulation and the PP level. The maturation of the aortic trunk and its branches results from adaptative mechanisms involving shear and tensile stress, with major potential consequences on heart rate control, transit of wave reflections, and coronary perfusion. An adequate optimization of the Windkessel function, and hence PP, diastolic coronary perfusion and CV survival needs a critical MAP level to be reached in each individual during the postnatal period. The achievement of this MAP level requires the development of multiple resistance segments of the microvascular network, particularly within the kidney. Translated in adult populations, this pathophysiological process gives rise to a Gaussian BP distribution, with individuals remaining in the same BP percentile from birth onward (BP tracking). We suggest that hypertension results from early developmental vascular mechanisms that direct BP toward the higher percentiles of the Gaussian distribution curve.

Vascular Development, Pulse Pressure, and the Mechanisms of Hypertension