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Published on: May 3, 2018
Vascular development, pulse pressure, and the mechanisms of hypertension
Michel E Safar1, Harry Struijker Boudier
1Diagnosis Center, Hôpital Hôtel-Dieu, 1, Place du Parvis Notre-Dame, 75181 Paris Cedex 04, France. michel.safar@htd.ap-hop-paris.fr
Insights
Hypertension may originate from early vascular development, influencing blood pressure (BP) percentiles from birth. Optimal cardiovascular survival depends on adequate mean arterial pressure (MAP) and pulse pressure (PP) post-birth.
Area of Science:
- Cardiovascular physiology
- Developmental biology
- Hypertension research
Background:
- Blood pressure (BP) comprises mean arterial pressure (MAP) and pulse pressure (PP), reflecting microvascular resistance and large artery stiffness, respectively.
- Cardiovascular (CV) survival around birth hinges on heart-aorta coupling, Windkessel function, aortic elastin, and PP.
- Vascular maturation involves adaptative responses to stress, impacting heart rate, wave reflections, and coronary perfusion.
Purpose of the Study:
- To explore the developmental origins of hypertension.
- To elucidate the relationship between early vascular development and adult blood pressure distribution.
- To highlight the critical role of postnatal MAP and PP in cardiovascular health.
Main Methods:
- Conceptual analysis of cardiovascular development and BP regulation.
- Review of physiological mechanisms linking vascular maturation to BP.
- Integration of developmental pathways with adult BP distribution models.
Main Results:
- Adequate Windkessel function and PP require a critical postnatal MAP level, influenced by microvascular network development (e.g., in the kidney).
- Early developmental vascular mechanisms can direct an individual's BP towards higher percentiles of a Gaussian distribution.
- Blood pressure tracking from birth suggests persistent developmental influences.
Conclusions:
- Hypertension may stem from early developmental vascular processes that establish an individual's position on the BP distribution curve.
- Optimizing the Windkessel function and ensuring adequate coronary perfusion during the postnatal period are crucial for long-term CV health.
- Understanding these early mechanisms is key to preventing and managing hypertension.
Abstract:
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.
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