Ace inhibition modulates the apoptosis-regulatory proteins bcl-2 and bax in vascular smooth muscle cells from spontanoeusly hypertensive rats (SHR)

The apoptosis suppressing gene bcl-2 encodes a protein that blocks apoptotic death. On the other hand, the bax gene encodes a dominant inhibitor of the bcl-2 protein. Since the regulation of apoptosis appears to be altered in vascular smooth muscle cells (SMC) from SHR, the percentages of these cells expressing the proteins bcl-2 and bax were assessed by immunohistochemistry in small coronary arteries (<300 μM) of 10 36-week old normotensive WKY rats, 10 36-week old SHR and 10 36-week old SHR treated with the ACE inhibitor quinapril (10 mg/Kg/day, orally) during 20 weeks. The density of SMC was assessed by morphometry. As compared to WKY, untreated SHR exhibited increased (P<0.05) number of SMC, increased (P<0.01) bcl-2, and unchanged bax. The number of SMC and the percentage of SMC expressing the bcl-2 protein were similar in treated SHR that in WKY. As compared to both WKY and untreated SHR, quinapril-treated SHR exhibited increased (P<0.05) bax. These results suggest that ACE inhibition stimulates bax protein and restores susceptibility to apoptosis in SMC of SHR.