Ferreira Patrícia Maria, Souza Dos Santos Robson Augusto, Campagnole-Santos Maria José
Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901 MG, Brazil.
Regul Pept. 2007 Jun 7;141(1-3):168-74. doi: 10.1016/j.regpep.2006.12.031. Epub 2007 Jan 20.
Ang-(3-7) is a fragment of the renin-angiotensin system that can be derived both from Ang II or Ang-(1-7). In the present study we determined the cardiovascular effects produced by angiotensin-(3-7) [Ang-(3-7)] microinjection into the rostral ventrolateral medulla (RVLM), a key region for the control of sympathetic drive to the periphery. RVLM microinjection of Ang-(3-7) (20, 40 or 80 ng) in male Wistar rats anesthetized with urethane produced significant increases in MAP (19+/-3.8 mm Hg, n=5; 16+/-1.6 mm Hg, n=15 and 11+/-1.2 mm Hg, n=4, respectively) as compared to saline (4+/-0.7 mm Hg, n=6). These alterations were similar to that induced by Ang-(1-7) (14+/-1.3 mm Hg, 40 ng; n=12) and Ang II (17+/-2.3 mm Hg, 40 ng; n=7). Microinjection of losartan (AT(1) receptor antagonist, 100 pmol) or A779 (selective Mas receptor antagonist, 100 pmol) did not alter the pressor effect caused by Ang-(3-7). Microinjection of an Ang-(3-7) analogue, d-Ala(7)-Ang-(3-7) (100 pmol), completely abolished the pressor effect caused by Ang-(3-7). These results suggest that Ang-(3-7) may be an additional peptide of the RAS to act as neuromodulator, at least at the RVLM. Further, the Ang-(3-7) pressor effect is not mediated by the interaction with AT(1) or the Ang-(1-7), Mas, receptors.
血管紧张素-(3-7)是肾素-血管紧张素系统的一个片段，它可以由血管紧张素II或血管紧张素-(1-7)产生。在本研究中，我们确定了向延髓头端腹外侧区（RVLM）微量注射血管紧张素-(3-7) [Ang-(3-7)]所产生的心血管效应，RVLM是控制外周交感神经驱动的关键区域。在用乌拉坦麻醉的雄性Wistar大鼠中，向RVLM微量注射Ang-(3-7)（20、40或80 ng），与注射生理盐水（4±0.7 mmHg，n = 6）相比，平均动脉压（MAP）显著升高（分别为19±3.8 mmHg，n = 5；16±1.6 mmHg，n = 15和11±1.2 mmHg，n = 4）。这些变化与血管紧张素-(1-7)（14±1.3 mmHg，40 ng；n = 12）和血管紧张素II（17±2.3 mmHg，40 ng；n = 7）诱导的变化相似。微量注射氯沙坦（AT(1)受体拮抗剂，100 pmol）或A779（选择性Mas受体拮抗剂，100 pmol）并没有改变Ang-(3-7)引起的升压效应。微量注射血管紧张素-(3-7)类似物d-Ala(7)-Ang-(3-7)（100 pmol）完全消除了Ang-(3-7)引起的升压效应。这些结果表明，血管紧张素-(3-7)可能是肾素-血管紧张素系统中另一种作为神经调节剂起作用的肽，至少在RVLM是这样。此外，血管紧张素-(3-7)的升压效应不是通过与AT(1)或血管紧张素-(1-7)、Mas受体相互作用介导的。
