Background: 

Recently high amount of NO has been shown to induce hsp70 expression in SMC. There are not enough data on increased expression of both iNOS and heat shock protein 70 (hsp70) in atherosclerotic vessels. Lacidipine, may affect several physiological and biochemical pathways in atherosclerosis.

Aim: 

The purpose of this study is to investigate the production of hsp70 and iNOS in atherosclerotic carotid arteries and the effect of lacidipine on these expressions.

Methods: 

White rabbits were either received lacidipine (5 mg/kg/day) or vehicle (%1 carboxymethylcelulose p.o.). On the 8th day, a non occlusive, soft silicon collar was positioned around the left carotid arteries. The right carotid arteries were sham-operated. Both carotid arteries were removed on the 22nd day. Expression and distribution of hsp70 and iNOS of the arteries were determined by immunohistochemistry. Intimal thickening were measured by computer based morphometric analysis.

Results: 

Lacidipine significantly inhibited the intimal thickening and index (intima/media) in collared arteries. Both hsp70 and iNOS expression were increased in smooth muscle layers of atherosclerotic carotid arteries and reversed back by lacidipine treatment.

Conclusions: 

We suggested that increased levels of iNOS, by producing high amount of NO, may also induce hsp70 expression in atherosclerotic carotid arteries. Lacidipine may have beneficial effect on pathogenesis of atherosclerosis by overcoming increased levels of these inflammatory proteins.