The effect of losartan on angiotensin II-induced cell proliferation in a rat aorta smooth muscle cell line

Abstract

The success of revascularization procedures is limited by recurrent stenosis, which is a narrowing of a blood vessels that results from neo-intimal hyperplasia. The renin-angiotensin-aldosterone system has been implicated in the pathogenesis of neo-intimal hyperplasia, and a role for angiotensin II in vascular smooth muscle cell proliferation has been proposed. There are at least two high-affinity subtypes of angiotensin II receptors, AT1 and AT2, both of which are seven-transmembrane G protein-coupled receptors. We investigated the effect of losartan, an AT1receptor antagonist, on vascular smooth muscle cell proliferation using the A7r5 smooth cell line derived from rat aorta. Losartan was shown to prevent angiotensin II-induced cell proliferation, thereby suggesting that the effect of angiotensin II was mediated via AT1 receptors. These data strengthen the concept that inhibitors of the reninangiotensin system can effectively prevent recurrent stenosis.

Preliminary insights into the action of non-antibiotic pharmaceuticals in the colonization of Pseudomonas aeruginosa TGC04

“…Thus, intact cells, i.e., those without damage to the wall or membrane, are more resistant (53). Losartan (54), dipyrone (55) and diclofenac (56) are hydrophobic, and losartan can also present acidic properties for weeks in aqueous solution. On the other hand, acetylsalicylic acid is amphiphilic (57), while metformin and paracetamol are hydrophilic (58,59).…”