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(Hypertension. 2009;54:203.)
© 2009 American Heart Association, Inc.

Brief Reviews

Sodium Intake and Vascular Stiffness in Hypertension

Michel E. Safar; Mohamed Temmar; Augustine Kakou; Patrick Lacolley; Simon N. Thornton

From the Faculty of Medicine (M.E.S.), Paris Descartes University, Hôtel-Dieu Hospital, AP-HP, Diagnosis Center, Paris, France; Cardiology Center (M.T.), Ghardaia, Algeria; Institut National de la Santé et de la Recherche Médicale U684 (A.K., P.L., S.N.T.), Vandoeuvre-les-Nancy, France; Université Henri Poincaré (A.K., P.L., S.N.T.), Nancy Université, Nancy, France.

Correspondence to Michel E. Safar, Diagnosis Center, Hôpital Hôtel-Dieu, 1 Place du Parvis Notre-Dame, 75181 Paris, Cedex 04, France. E-mail michel.safar@htd.aphp.fr

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The relationship between sodium and blood pressure (BP) continues to be the focus of intense research. In humans, the impact of sodium on systolic BP (SBP), diastolic BP (DBP), mean BP, and pulse pressure (PP) is currently thought to be quite similar for the 4 pressures and to occur practically with identical consequences (see reviews^1–8). In this review, the effect of sodium on SBP is taken into consideration mainly for a very simple but important reason: in recent years, SBP and PP have become the parameters the most difficult to control in hypertensive subjects, which is the principal goal of most antihypertensive drugs.¹

Central (aortic) SBP is a complex parameter that is influenced both by cardiac (stroke volume and ventricular ejection) and vascular (arterial and venous stiffness and wave reflections) factors.¹ Stroke volume, the ratio between cardiac output and heart rate, depends not only on cardiac structure and function but also on venous return. Through the extracellular and intravascular spaces and their elastic properties, stroke volume and, hence, SBP are strongly associated with sodium balance, ie, with the relationship between sodium intake and its urinary elimination, and, finally, the traditional pressure-diuresis mechanism.⁴ This pathway, which mainly affects the venous circulation, requires a low and steady BP, together with a vast storage capacity for salt and water. Another important pathway affects the high-pressure pulsatile arterial system, in which the SBP level is achieved through increased arterial stiffness and disturbed wave reflections. These hemodynamic parameters are strongly influenced by sodium intake, . . . [Full Text of this Article]

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