title: Arterial stiffness in hypertensive subjects with or without end-stage renal disease.
abstract: Therapeutic trials have shown that the response to antihypertensive drug treatment is heterogeneous, with substantially higher effects of cardiovascular prevention for the cerebral than for the coronary circulation. This finding suggests that the response of large conduit arteries to elevated blood pressure may vary greatly between the different compartments of the arterial bed. Recent in vivo non-invasive studies in humans suggest that the stiffness of large arteries in subjects with essential hypertension differs greatly according to the vascular territory involved. Operational arterial stiffness, i.e., measured at the mean blood pressure of the hypertensive population by comparison with normotensive subjects, is increased in central arteries (carotid artery, aorta) but normal in peripheral muscular arteries (femoral artery, radial artery). On the other hand, when hypertensive and normotensive subjects are compared for the same blood pressure, arterial stiffness appears to be normal for the radial artery but decreased for the femoral artery and the aorta. In the case of carotid arteries, isobaric arterial stiffness is normal in subjects with uncomplicated essential hypertension but decreased in hypertensive patients with end-stage renal disease. Thus, important differences may be observed according to the territory involved, suggesting that the response to drug treatment of hypertension may be influenced not only by the blood pressure reduction itself but also by the regional properties of each particular vascular bed and the presence of advanced renal disease.
authors.affiliation: Department of Internal Medicine, Broussais Hospital, Paris, France.
authors.forename: M E
authors.initials: ME
authors.lastname: Safar
authors.forename: G M
authors.initials: GM
authors.lastname: London
mesh_terms: D001158:Arteries / Q000503:physiopathology*; D004548:Elasticity; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000209:etiology*