De Maria Marilda L A, Araújo Liliane D, Fraga-Silva Rodrigo A, Pereira Letícia A S, Ribeiro Heder J, Menezes Gustavo B, Shenoy Vinayak, Raizada Mohan K, Ferreira Anderson J
Department of Morphology - Av. Antônio Carlos, 6627 - ICB - UFMG 31.270-901 - Belo Horizonte, MG, Brazil.
Protein Pept Lett. 2016;23(1):9-16. doi: 10.2174/0929866522666151013130550.
Previous studies have shown that activation of endogenous angiotensin-converting enzyme 2 (ACE2) results in various beneficial effects in the cardiovascular system. Recently, a new ACE2 activator, named diminazene aceturate (DIZE), was described. Here, we evaluated the actions of this compound in blood pressure (BP) and heart rate (HR) of conscious normotensive and hypertensive rats, as well as explored its mechanism of actions using isolated vessels. The renovascular model of hypertension was utilized. The participation of the Angiotensin-(1-7) receptor Mas and nitric oxide (NO) in the effects of DIZE was evaluated using A-779 and L-NAME, respectively. It was observed that DIZE caused a marked decrease in BP with a compensatory increase in HR in nornotensive rats. Accordingly, a significant reduction in the blood flow of the mesenteric bed was evidenced using intravital microscopy. Moreover, in rats with renovascular hypertension, DIZE caused a decrease in BP similar to the hypotensive effect induced by captopril. Importantly, this compound also prevented the development of cardiac hypertrophy induced by hypertension. The isolated vessels technique revealed that the vasodilator effects of DIZE were dependent on Mas activation and NO release. Thus, our findings demonstrated that DIZE reduces the BP of normotensinve and hypertensive rats possibly by a mechanism involving Mas and NO.
先前的研究表明,内源性血管紧张素转换酶2(ACE2)的激活在心血管系统中会产生多种有益作用。最近,一种名为乙酰马嗪(DIZE)的新型ACE2激活剂被报道。在此,我们评估了该化合物对清醒正常血压和高血压大鼠血压(BP)和心率(HR)的影响,并利用离体血管探究其作用机制。采用肾血管性高血压模型。分别使用A-779和L-NAME评估血管紧张素-(1-7)受体Mas和一氧化氮(NO)在DIZE作用中的参与情况。结果观察到,DIZE使正常血压大鼠的血压显著降低,同时心率代偿性增加。相应地,通过活体显微镜观察证实肠系膜床血流量显著减少。此外,在肾血管性高血压大鼠中,DIZE引起的血压降低与卡托普利诱导的降压作用相似。重要的是,该化合物还可预防高血压诱导的心脏肥大的发展。离体血管技术显示,DIZE的血管舒张作用依赖于Mas激活和NO释放。因此,我们的研究结果表明,DIZE可能通过涉及Mas和NO的机制降低正常血压和高血压大鼠的血压。