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(Hypertension. 2001;38:1416.)
© 2001 American Heart Association, Inc.

Fourth Workshop on Structure and Function of Large Arteries: Part III

Pulse Pressure, Endothelium Function, and Arterial Stiffness in Spontaneously Hypertensive Rats

Michel Safar; Philippe Chamiot-Clerc; Georges Dagher; Jean François Renaud

From the Department of Internal Medicine and INSERM U337, Broussais Hospital (M.S., G.D.), Paris, France; and the Medical Research Department, Marie-Lannelongue Hospital (P.C.-C., J.F.R.), Le Plessis-Robinson, France.

Reprint requests to Prof Michel Safar, Médecine Interne 1, Groupe Hospitalier Broussais–G. Pompidou, Hôpital Broussais, 96 rue Didot, 75674 Paris, Cedex 14, France. E-mail michel.safar{at}brs.ap-hop-paris

Abstract

In rats, removal of the carotid arterial or abdominal aortic endothelium results in an acute increase of diameter and compliance. In humans, acute local administration of a specific NO synthase inhibitor increases radial artery compliance but not the diameter. The purpose of this review is to determine whether in spontaneously hypertensive rats (SHR), a cause-and-effect relationship may be observed between endothelial function and arterial stiffness with possible consequences on pulse pressure (PP) control. The study is based on a comparative time-dependent analysis of the following in young and old SHR: aortic blood pressure measurements and reactivity, ultrasonographic arterial stiffness assessment, aortic histomorphometry and staining, and molecular biology with evaluation of endothelium function. In young SHR, aortic mean blood pressure and PP increase proportionally, whereas isobaric arterial stiffness is unchanged or poorly modified. The endothelial NO response to norepinephrine is normal or upregulated as a response to predominant vasoconstrictive influences. In contrast, in old SHR, PP and mean blood pressure change disproportionately with age, together with an enhanced isobaric arterial stiffness. The endothelial NO response to norepinephrine is abolished, in association with endothelium-dependent heightened norepinephrine reactivity and enhanced accumulation of vessel extracellular matrix. In this latter case, exogenous NO acutely and selectively lowers the increased PP. Thus, during SHR aging, a negative feedback may be observed between NO bioactivity and PP through changes in arterial structure and function. Whether this alteration contributes to the development of systolic hypertension in old populations remains to be determined.

Key Words: rats, inbred SHR • arteries • endothelium • nitric oxide

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