Experimental Vasoprotection by Calcium Antagonists Against Calcium-Mediated Arteriosclerotic Alterations

Human Vascular Smooth Muscle Cells Undergo Vesicle-Mediated Calcification in Response to Changes in Extracellular Calcium and Phosphate Concentrations

“…However, our present data clearly show that cell death is not the only mechanism responsible for VSMC calcification, because we were able to distinguish AB from MV and demonstrate that both are capable of initiating calcification, albeit by possibly different mechanisms. In our experiments, VSMC apoptosis was rare in the presence of serum, whereas MV were released by viable VSMC, particularly in the presence of elevated levels of extracellular Ca and P. Vesicle release by VSMC has been described in vivo in a number of conditions, including atherosclerosis, hypertension, and Ca overload induced by vitamin D 3 toxicity (27)(28)(29). It has been suggested that Ca-loaded vesicles are released from VSMC to protect against the cytotoxic effects of intracellular Ca overload (29).…”

“…In our experiments, VSMC apoptosis was rare in the presence of serum, whereas MV were released by viable VSMC, particularly in the presence of elevated levels of extracellular Ca and P. Vesicle release by VSMC has been described in vivo in a number of conditions, including atherosclerosis, hypertension, and Ca overload induced by vitamin D 3 toxicity (27)(28)(29). It has been suggested that Ca-loaded vesicles are released from VSMC to protect against the cytotoxic effects of intracellular Ca overload (29). Our data showing that VSMC increased vesicle release in response to extracellular Ca and remained viable within the calcified matrix supports this notion but suggests that if phagocytosis were limited, then the extracellular accumulation of these vesicles, particularly in the context of elevated Ca and P, would lead to calcification.…”

Multifunctional Roles for Serum Protein Fetuin-A in Inhibition of Human Vascular Smooth Muscle Cell Calcification

“…Vesicle release by VSMC is thought to be a protective mechanism used to remove excess intracellular Ca to prevent overload and subsequent apoptosis (29). In this study, we demonstrate that the circulating protein, fetuin-A, potentially plays multiple roles in protecting VSMC from the detrimental effects of Ca overload and subsequent calcification.…”

Nifedipine Enhances the Cardioprotective Effect of an Angiotensin-II Receptor Blocker in an Experimental Animal Model of Heart Failure

“…Such increased availability of NO may contribute to the beneficial effects of CCBs that have been found by others, including antiplatelet (27,28), antiproliferative (29,30), and antiatherosclerotic effects (31−33). In our study, treatment with nifedipine decreased plasma TBARS and decreased 4-HNE in the LV myocardium, which means that the oxidative stress in heart failure was decreased by CCB therapy (Table 1, Figs.…”