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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/H1567    most recent 00622.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Lacolley, P. Articles by Frohlich, E. D. PubMed PubMed Citation Articles by Lacolley, P. Articles by Frohlich, E. D.

REVIEW

Angiotensin II, mechanotransduction, and pulsatile arterial hemodynamics in hypertension

¹Université Henri Poincaré, Institut National de la Santé et de la Recherche Médicale U961, Nancy, France; ²Université Paris Descartes, Assistance Publique-Hôpitaux de Paris, Hôtel-Dieu Centre de Diagnostic et de Thérapeutique, Paris, France; and ³Ochsner Clinic Foundation, New Orleans, Louisiana

Submitted July 10, 2009 ; accepted in final form September 4, 2009

ABSTRACT

The aortic blood pressure curve involves two components: a steady component, the mean arterial pressure (MAP), which is dependent on cardiac output and vascular resistance, and a pulsatile component pulse pressure (PP), which is dependent on arterial stiffness and pulse wave reflections. The transduction mechanisms of MAP and PP differ markedly, involving focal adhesion kinase for MAP and oxygen free radicals for PP. Angiotensin II (ANG II) and its blockade are associated with changed vascular resistance and MAP; however, their effects on PP (peripheral and mostly central PP) have been inadequately investigated. In hypertensive rats, when compared with their normotensive controls, ANG II blockade normalizes central PP (<50 mmHg) but not MAP when the same drug dosage is used for each. In hypertensive patients, ANG II blockade reduces arterial stiffness and pulse wave reflections, but with the same reduction in MAP, there is a greater reduction in central than peripheral PP, thereby increasing carotid-brachial PP amplification. With long-term ANG II blockade, the hypertensive arteriolar hypertrophy observed at baseline is corrected in association with reduced arteriolar reflection coefficients, reduced carotid arterial attachments linking ₅-integrin to its ligand fibronectin, and decreased circulating C-reactive protein. When given a normal salt diet, each of these factors contributes separately in reducing arterial stiffness and wave reflections. These responses disappear with a high-salt diet, a condition that usually involves the activation of the local vascular renin-angiotensin-aldosterone system and can be prevented by its selective blockade. Thus ANG II inhibition seems to contribute independently in reducing central PP and aortic stiffness.

antihypertensive therapy; pulsatile forces