Effect of bradykinin on gene expression in human aortic smooth muscle cells

The renin-angiotensin system and angiotensin-converting enzyme (ACE) are increasingly being implicated in the pathogenesis of artery disease and its sequelae. ACE inhibitors prevent stimulation of smooth muscle cell angiotensin II receptors, thereby blocking both contractile and proliferative actions of angiotensin II. In addition, ACE inhibition of kininase inhibits the breakdown of bradykinin, a direct stimulant of nitric oxide release from the intact endothelial cells. Thus, at the cellular level ACE inhibition shifts the balance of ongoing mechanisms in favor of those promoting vasodilatory, anti-aggregatory, antithrombotic and antiproliferative effects. The purpose of this study was to examine the effects of bradykinin on gene expression in vascular smooth muscle cells. We used DNA microarray technology to identify differentially expressed genes in smooth muscle cells exposed to bradykinin. The gene expression profile elucidates new aspects of therapy by ACE inhibitors.