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Cardiovascular Research Advance Access first published online on August 7, 2008
This version [Corrected Proof] published online on August 25, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn211
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Enhanced pulsatile pressure accelerates vascular smooth muscle migration: implications for atherogenesis of hypertension

Tomohiro Tada, Jun Nawata*, Huan Wang, Noriko Onoue, Doe Zhulanqiqige, Kenta Ito, Koichiro Sugimura, Yoshihiro Fukumoto and Hiroaki Shimokawa

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai 980-8574, Japan

* Corresponding author. Tel: +81 22 717 7153; fax: +81 22 717 7156. E-mail address: nawata{at}cardio.med.tohoku.ac.jp

Aims: Clinical studies have suggested that pulsatile pressure is an independent risk factor for atherosclerosis. However, it is unknown whether enhanced pulsatile pressure per se directly accelerates vascular smooth muscle cell (VSMC) migration, an important process of atherosclerosis.

Methods and results: Using our original Pressure-loading system with a Boyden chamber, we examined the direct effects of variable pressures and pulse rates on migration of rat aortic VSMCs in vitro. High pulse pressure (180/90 mmHg, pulsatile vs. 180 mmHg, static), high mean pressure (180/90 vs. 90/0 mmHg, with the same pulse pressure), wide pulse pressure (190/110 vs. 170/130 mmHg, with the same mean pressure), and high pulse rate (120 vs. 40 per min) significantly accelerated the VSMC migration (1.35, 2.38, 1.38 and 1.27-fold, respectively). The increase in intracellular calcium levels measured by fura-2/AM fluorescence was proportional to the magnitude of pressure loaded. The pressure-promoted VSMC migration was significantly inhibited by a phospholipase-C inhibitor U-73122 or a calmodulin inhibitor W-7. Inositol 1,4,5-trisphosphate receptor blockers 2-aminoethoxydiphenyl borate or xestospongin-C significantly inhibited the VSMC migration, whereas a ryanodine receptor blocker ryanodine had no effects. Furthermore, a calcium channel blocker (CCB), azelnidipine, and an angiotensin type-1 receptor blocker, olmesartan, also significantly inhibited the VSMC migration.

Conclusion: These results provide direct evidence for the pro-atherogenic effects of enhanced pulsatile pressure and also suggest that the anti-atherogenic actions of CCBs and angiotensin type-1 receptor blockers are mediated in part by their direct inhibitory effects on VSMC migration in addition to their anti-hypertensive effects.

KEYWORDS Pulsatile pressure; Vascular smooth muscle cell; Migration; Calcium

Time for primary review: 21 days


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