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The intracellular renin-angiotensin effectors (peptides, enzymes, receptors) and their effects are intriguing for a lot of systems. That’s why we aimed the effects of intracellularly-administered angiotensins (angiotensin II, angiotensin III, angiotensin IV, angiotensin fragment 1-7), angiotensinogen, CGP-42112A, apelin, and angiotensin receptors blockers (losartan, PD123319), by the means of liposomes, on apoptosis of cultured isolated rat aortic vascular smooth muscle cells. We evidenced that CGP-42112A (a potent AT2 angiotensin II receptor agonist), administered intracellularly, induced the apoptosis of the cultured isolated vascular smooth muscle cells in a much higher proportion than other agonists and antagonists of angiotensin system: CGP-42112A> angiotensin II> angiotensin III≅ angiotensinogen. Moreover, losartan (an AT1 angiotensin II receptor antagonist), administered intracellularly, induced an important degree of apoptosis of cultured isolated vascular smooth muscle cells. Losartan, administered as concomitant treatment for other angiotensin peptides and CGP-42112A, did not significantly modified the apoptotic effects of these peptides. On the other hand, PD123319 (an AT2 angiotensin II receptor antagonist) was able to significantly reduce the losartan effects when administered as co-treatment for 24 h. The same effects were obtained when LY294002, a PI3K/Akt signaling inhibitor, was administered as a co-treatment. We can conclude an involvement of an AT2 angiotensin II receptor and PI3K/Akt signaling in these apoptotic effects induced by some angiotensin peptides and losartan on cultured isolated rat aortic vascular …