The renin-angiotensin system and sodium may modulate age-related increases in pulse pressure and aortic rigidity, suggesting potential for antihypertensive drugs to attenuate arterial stiffness.
The renin-angiotensin system and genetic factors play a key role in arterial stiffness in elderly patients with systolic hypertension, suggesting potential targets for future antihypertensive therapies.
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.
M. E. Safar (Sat,) conducted a review in Systolic hypertension in the elderly. Renin-angiotensin system and sodium was evaluated. The renin-angiotensin system and sodium may modulate age-related increases in pulse pressure and aortic rigidity, suggesting potential for antihypertensive drugs to attenuate arterial stiffness.