Verapamil inhibits calcification and matrix vesicle activity of bovine vascular smooth muscle cells

Neal X. Chen, Fatih Kircelli, Kalisha D. O'Neill, Xianming Chen, Sharon M. Moe

Research output: Contribution to journalArticle

32 Scopus citations


Calcium channel activity in vascular smooth muscle cells is a critical component during vascular calcification and formation of matrix vesicles. Here, we examined whether the blockade of L-type calcium channels inhibits these functions. Bovine vascular smooth muscle cells or rat aorta organ cultures were incubated in media known to promote calcification and treated with the L-type calcium channel inhibitors verapamil, nifedipine, or nimodipine. The phenylalkylamine, verapamil, significantly decreased calcification of the vascular smooth muscle cells and rat aorta, in a dose-dependent manner, whereas the dihydropyridines, nifedipine and nimodipine, had no effect. Furthermore, verapamil, but not nifedipine, significantly decreased the alkaline phosphatase activity of bovine vascular smooth muscle cells. Verapamil pretreatment of the cells also inhibited matrix vesicle alkaline phosphatase activity and reduced the ability of these matrix vesicles to subsequently calcify on a type I collagen extracellular matrix scaffold. As L-type channels are blocked by verapamil and dihydropyridines, we suggest that verapamil inhibits vascular smooth muscle mineralization and matrix vesicle activity by mechanisms other than the simple blockade of this calcium channel activity.

Original languageEnglish (US)
Pages (from-to)436-442
Number of pages7
JournalKidney international
Issue number5
StatePublished - Mar 1 2010


  • Calcium
  • Cell signaling
  • Mineral metabolism
  • Vascular calcification

ASJC Scopus subject areas

  • Nephrology

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