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Research Article Free access | 10.1172/JCI118807

Chronic blockade of AT2-subtype receptors prevents the effect of angiotensin II on the rat vascular structure.

B I Levy, J Benessiano, D Henrion, L Caputo, C Heymes, M Duriez, P Poitevin, and J L Samuel

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

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Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Benessiano, J. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Henrion, D. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Caputo, L. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Heymes, C. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Duriez, M. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Poitevin, P. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale, Unit 141, Université Denis Diderot, Paris, France.

Find articles by Samuel, J. in: JCI | PubMed | Google Scholar

Published July 15, 1996 - More info

Published in Volume 98, Issue 2 on July 15, 1996
J Clin Invest. 1996;98(2):418–425. https://doi.org/10.1172/JCI118807.
© 1996 The American Society for Clinical Investigation
Published July 15, 1996 - Version history
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Abstract

Angiotensin II (Ang II) is both a vasoactive and a potent growth-promoting factor for vascular smooth muscle cells. Little is known about the in vivo contribution of AT1 and AT2 receptor activation to the biological action of Ang II. Therefore, we investigated the effect of AT1 or AT2 subtype receptor chronic blockade by losartan or PD123319 on the vascular hypertrophy in rats with Ang II-induced hypertension. Normotensive rats received for 3 wk subcutaneous infusions of Ang II (120 ng/kg per min), or Ang II + PD 123319 (30 mg/kg per d), or Ang II + losartan (10 mg/kg per d) or PD 123319 alone, and were compared with control animals. In normotensive animals, chronic blockade of AT2 receptors did not affect the plasma level of angiotensin II and the vascular reactivity to angiotensin II mediated by the AT1 receptor. Chronic blockade of AT1I in rats receiving Ang II resulted in normal arterial pressure, but it induced significant aortic hypertrophy and fibrosis. Chronic blockade of AT2 receptors in Ang II-induced hypertensive rats had no effect on arterial pressure, but antagonized the effect of Ang II on arterial hypertrophy and fibrosis, suggesting that in vivo vasotrophic effects of Ang II are at least partially mediated via AT2 subtype receptors.

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