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(Hypertension. 2006;48:404.)
© 2006 American Heart Association, Inc.
Original Articles |
From the Cardiovascular Division, Kings College London School of Medicine, St Thomas Hospital, London, United Kingdom.
Correspondence to Philip J. Chowienczyk, Department of Clinical Pharmacology, St Thomas Hospital, Lambeth Palace Rd, London SE1 7EH, United Kingdom. E-mail phil.chowienczyk{at}kcl.ac.uk
Stiffness of large elastic arteries is elevated in subjects with hypertension, an effect that could potentially be explained by increased distending pressure. We examined effects of an acute change in blood pressure on carotid-femoral pulse wave velocity and carotid artery distensibility (inversely related to stiffness) in normotensive control subjects (n=20, mean age 42) with mean arterial pressure (MAP) 84±1.7 mm Hg (mean±SE) and subjects with essential hypertension (n=20, mean age 45, MAP 104±2.0 mm Hg). Normotensive subjects received intravenous nitroglycerin (NTG) and angiotensin II to lower/increase blood pressure. Hypertensive subjects received NTG to lower blood pressure. Pulse wave velocity was 24% (95% CI: 12% to 35%) higher and carotid distensibility 47% (95% CI: 32% to 63%) lower in hypertensive subjects compared with controls. In normotensive subjects, acute changes in blood pressure produced expected changes in stiffness. However, in hypertensive subjects, despite reducing MAP by 22 mm Hg to the same level as in normotensive subjects, there was no detectable reduction in arterial stiffness: pulse wave velocity remained 24% (95% CI: 10% to 38%) higher and carotid distensibility 48% (95% CI: 31% to 63%) lower in hypertensive compared with normotensive subjects. Because blood pressureindependent effects of NTG are, if anything, to reduce stiffness, these results indicate that elevated carotid and aortic stiffness in hypertensive subjects is not explained by elevated blood pressure but relates to structural change in the arterial wall.
Key Words: arterial pressure carotid arteries hypertension, arterial
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