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Published on: December 2, 2014
Acute reduction of blood pressure by nitroglycerin does not normalize large artery stiffness in essential
Andrew D Stewart1, Benyu Jiang, Sandrine C Millasseau
1Cardiovascular Division, King's College London School of Medicine, St Thomas' Hospital, London, United Kingdom.
Insights
Arterial stiffness is higher in hypertension, but not due to blood pressure. Structural changes in the arterial wall, not elevated pressure, explain this increased stiffness in hypertensive individuals.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Arterial Biomechanics
Background:
- Elevated large elastic artery stiffness is a hallmark of hypertension.
- Increased arterial stiffness may be attributed to sustained higher distending pressures.
Purpose of the Study:
- To investigate whether acute changes in blood pressure affect arterial stiffness differently in normotensive versus hypertensive individuals.
- To determine if elevated arterial stiffness in hypertension is solely due to increased blood pressure or involves structural alterations.
Main Methods:
- Carotid-femoral pulse wave velocity and carotid artery distensibility were measured in normotensive and hypertensive subjects.
- Blood pressure was acutely manipulated using intravenous nitroglycerin and angiotensin II in normotensive subjects, and nitroglycerin in hypertensive subjects.
Main Results:
- Hypertensive subjects exhibited significantly higher pulse wave velocity and lower carotid distensibility compared to normotensive controls.
- Acute blood pressure reduction in hypertensive subjects did not normalize arterial stiffness, which remained significantly elevated.
- In normotensive subjects, acute blood pressure changes induced expected alterations in arterial stiffness.
Conclusions:
- Elevated arterial stiffness in hypertension is not explained by acute changes in blood pressure.
- Structural changes within the arterial wall, independent of distending pressure, are likely responsible for increased stiffness in hypertensive individuals.
Abstract:
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 pressure-independent 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.
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