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Poster Abstract PresentationsSession Title: Poster Session II

Abstract 461: Cilnidipine Attenuated Angiotensin II-induced Abdominal Aortic Aneurysms in Apolipoprotein E-deficient Mice

Yuki Kakio, Haruhito A Uchida, Ryoko Umebayashi, Jun Wada
Arteriosclerosis, Thrombosis, and Vascular Biology. 2015;35:A461
Yuki Kakio
Medicine and Clinical Science, Okayama Univ Grad Schl of Med, Okayama, Japan
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Haruhito A Uchida
Chronic Kidney Disease and Cardiovascular Disease, Okayama Univ Grad Schl of Med, Okayama, Japan
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Ryoko Umebayashi
Medicine and Clinical Science, Okayama Univ Grad Schl of Med, Okayama, Japan
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Jun Wada
Medicine and Clinical Science, Okayama Univ Grad Schl of Med, Okayama, Japan
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Abstract

Objective: Chronic infusion of angiotensin II (AngII) promotes development of abdominal aortic aneurysms (AAAs) in hypercholesterolemic mice. Previous studies have shown that local inflammation and increased oxidative stress plays an important role on formation of AAAs. In addition, it is reported that voltage-dependent N-type Ca2+ channels in endothelial cells contribute to oxidative stress-related endothelial dysfunction induced by AngII in mice. Therefore, we hypothesized that cilnidipine, an N/L-type calcium channel blocker, exerts vasoprotective effect by inhibiting inflammation and superoxide generation in mice. The purpose of this study was to evaluate whether cilnidipine influenced AngII-induced AAAs.

Methods and Results: Male apolipoprotein E deficient mice (8-12 weeks old) were fed a normal laboratory diet. Mice were infused subcutaneously with either cilnidipine or vehicle by osmotic minipumps. Three days later, mice were also infused subcutaneously with either AngII (1,000 ng/kg/min, n = 14-16) or saline (n = 4) each by osmotic minipumps for 4 weeks. AngII increased systolic blood pressure. Cilnidipine decreased blood pressure in AngII-infused mice, but had not effect during saline infusion. AngII infusion did not alter serum cholesterol concentrations. However, cilnidipine slightly decreased serumcholesterol concentrations in AngII-infused mice. Cilnidipine had no effect on body weights, heart rates, and urine total protein, but mildly restored plasma renin activity that were suppressed by AngII infusion. Cilnidipine did not affect ex vivo measurement of maximal diameter of abdominal aorta (1.04 ± 0.09 mm vs 1.11 ± 0.06 mm, n.s.) in saline infused mice. AngII infusion significantly increased ex vivo maximal diameters of abdominal aortas, but was attenuated by cilnidipine (1.79 ± 0.59 mm vs 1.26 ± 0.38 mm, P < 0.05). In addition, cilnidipine significantly reduced the incidence of AngII-induced AAAs (Cilnidipine: 38 %, Vehicle: 88 %; P < 0.05). Furthermore, gelatin zymography demonstrated that cilnidipine diminished AngII-induced increase in aortic MMP-9 protein abundance.

Conclusion: Cilnidipine attenuated AngII-induced AAAs in male apolipoprotein E deficient mice.

  • Abdominal aortic aneurysm
  • Cardiovascular disease
  • Author Disclosures: Y. Kakio: None. H.A. Uchida: None. R. Umebayashi: None. J. Wada: None.

  • © 2015 by American Heart Association, Inc.
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May 2015, Volume 35, Issue Suppl 1
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    Abstract 461: Cilnidipine Attenuated Angiotensin II-induced Abdominal Aortic Aneurysms in Apolipoprotein E-deficient Mice
    Yuki Kakio, Haruhito A Uchida, Ryoko Umebayashi and Jun Wada
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2015;35:A461, originally published August 11, 2015

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    Abstract 461: Cilnidipine Attenuated Angiotensin II-induced Abdominal Aortic Aneurysms in Apolipoprotein E-deficient Mice
    Yuki Kakio, Haruhito A Uchida, Ryoko Umebayashi and Jun Wada
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2015;35:A461, originally published August 11, 2015
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