Upregulation of Endothelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors

    loading  Checking for direct PDF access through Ovid

Abstract

Background

Oxidized low-density lipoprotein (ox-LDL) causes endothelial dysfunction in part by decreasing the availability of endothelial nitric oxide (NO). Although HMG CoA reductase inhibitors restore endothelial function by reducing serum cholesterol levels, it is not known whether they can also directly upregulate endothelial NO synthase (ecNOS) activity.

Conclusions

Inhibition of endothelial HMG CoA reductase upregulates ecNOS expression predominantly by posttranscriptional mechanisms. These findings suggest that HMG CoA reductase inhibitors may have beneficial effects in atherosclerosis beyond that attributed to the lowering of serum cholesterol by increasing ecNOS activity. (Circulation. 1998;97:1129-1135.)

Related Topics

    loading  Loading Related Articles