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The mechanism(s) of systolic hypertension in the elderly imply structural and functional alterations of the large artery wall. Clinical and experimental studies have shown that, in the long term, the renin-angiotensin system may act on the geometry and stiffness of the large artery wall independently of blood pressure level through alterations of the extracellular matrix of vascular smooth muscle cells. In humans, gene polymorphisms related to angiotensin type I receptors, sodium, or alterations of endothelial function may modulate the age-related increase in pulse pressure and aortic rigidity, the two main predictors of cardiovascular risk in the elderly. Based on this approach to the renin-angiotensin system, it is suggested that antihypertensive drugs may be developed that attenuate the increase of aortic rigidity with age, acting on the hormonal environment as well as the secretory properties of vascular smooth muscle cells.

Factors influencing arterial stiffness in systolic hypertension in the elderly: role of sodium and the renin-angiotensin system