Background: Vascular calcification is an organized process in which vascular smooth muscle cells (VSMCs) are implicated primarily. The purpose of the present study was to assess the effects of calcium antagonists and statins on VSMC calcification in vitro.
Methods: VSMC calcification was stimulated by incubation in growth medium supplemented with 10 mmol/l beta-glycerophosphate, 8 mmol/l CaCl(2), 10 mmol/l sodium pyruvate, 1 micromol/l insulin, 50 microg/ml ascorbic acid, and 100 nmol/l dexamethasone (calcification medium).
We investigated the pleiotropic effects of a calcium antagonist (amlodipine) on early atherosclerosis development in the presence and absence of an HMG-CoA-reductase inhibitor (atorvastatin) in apolipoprotein E*3-Leiden/human C-reactive protein (E3L/CRP) transgenic mice. Male E3L/CRP transgenic mice were fed a cholesterol-containing diet either with or without amlodipine and/or atorvastatin. After 31 weeks, atherosclerosis in the aortic root area was quantified.
View Article and Find Full Text PDFPurpose Of Review: C-reactive protein (CRP) is consistently associated with cardiovascular disease in prospective and cross-sectional clinical and epidemiological studies. Inflammation is an important mechanism in cardiovascular disease, and the plasma level of CRP is considered to reflect the inflammatory condition of the patient and/or the vessel wall. In addition, there are also a number of indications for a causal role of CRP in cardiovascular disease.
View Article and Find Full Text PDFVascular calcification is a prominent feature of atherosclerosis but the mechanisms underlying vascular calcification are still obscure. Since bone-associated proteins such as osteonectin, osteocalcin, and matrix Gla protein have been detected in calcified vascular tissues, calcification has been considered to be an organized, regulated process similar to mineralization in bone tissue. Vascular smooth muscle cells (VSMCs) are currently considered to be responsible for the formation of vascular calcifications.
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