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(Hypertension. 1995;26:963-970.)
© 1995 American Heart Association, Inc.
Articles |
From Laboratoire de Pharmacologie Cardiovasculaire, Faculté de Pharmacie (R.T.-T., N.N., F.A., T.M., J.A.), and INSERM U308 (P.T.), Nancy, France.
Correspondence to Jeffrey Atkinson, PhD, Laboratoire de Pharmacologie Cardiovasculaire, Faculté de Pharmacie, 5 rue Albert Lebrun, 54000 Nancy, France.
Abstract We tested whether cardiac mass can be related to decreased aortic stiffness in an original rat model of isolated systolic hypertension. Increased aortic stiffness was produced by calcium overload of elastic arteries after vitamin D3 plus nicotine treatment. Half of the animals were chronically treated with the angiotensin-converting enzyme inhibitor perindopril (1 mg/kg per day PO). Rats were pithed, and lower body vascular resistance was measured. Blood pressure was then increased by phenylephrine infusion, and carotidofemoral pulse wave velocity was measured. This value together with those for thoracic aorta internal diameter and medial thickness (determined after in situ fixation and histomorphometry) were used to calculate elastic modulus. Vitamin D3 plus nicotine treatment produced parallel increases in cardiac mass and elastic modulus, with a significant correlation between the two. There was no significant change in resistance. Treatment with perindopril reversed the changes in cardiac mass and elastic modulus but had no effect on resistance after calcium overload of the elastic arteries. In this model of isolated systolic hypertension, we showed that cardiac mass is related to arterial elasticity.
Key Words: angiotensin-converting enzyme inhibitor elasticity hypertrophy, left ventricular
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