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首页> 外文期刊>American Journal of Physiology >Intrarenal mouse renin-angiotensin system during ANG II-induced hypertension and ACE inhibition.
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Intrarenal mouse renin-angiotensin system during ANG II-induced hypertension and ACE inhibition.

机译：肾内小鼠肾素-血管紧张素系统在ANG II诱导的高血压和ACE抑制期间。

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摘要

Angiotensin-converting enzyme (ACE) inhibition (ACEi) ameliorates the development of hypertension and the intrarenal ANG II augmentation in ANG II-infused mice. To determine if these effects are associated with changes in the mouse intrarenal renin-angiotensin system, the expression of angiotensinogen (AGT), renin, ACE, angiotensin type 1 receptor (AT(1)R) mRNA (by quanitative RT-PCR) and protein [by Western blot (WB) and/or immunohistochemistry (IHC)] were analyzed. C57BL/6J male mice (9-12 wk old) were distributed as controls (n = 10), ANG II infused (ANG II = 8, 400 ng x kg(-1) x min(-1) for 12 days), ACEi only (ACEi = 10, lisinopril, 100 mg/l), and ANG II infused + ACEi (ANG II + ACEi = 11). When compared with controls (1.00), AGT protein (by WB) was increased by ANG II (1.29 +/- 0.13, P < 0.05), and this was not prevented by ACEi (ACEi + ANG II, 1.31 +/- 0.14, P < 0.05). ACE protein (by WB) was increased by ANG II (1.21 +/- 0.08, P < 0.05), and it was reduced by ACEi alone (0.88 +/- 0.07, P < 0.05) or in combination with ANG II (0.80 +/- 0.07, P < 0.05). AT(1)R protein (by WB) was increased by ANG II (1.27 +/- 0.06, P < 0.05) and ACEi (1.17 +/- 0.06, P < 0.05) but not ANG II + ACEi [1.15 +/- 0.06, not significant (NS)]. Tubular renin protein (semiquantified by IHC) was increased by ANG II (1.49 +/- 0.23, P < 0.05) and ACEi (1.57 +/- 0.15, P < 0.05), but not ANG II + ACEi (1.10 +/- 0.15, NS). No significant changes were observed in AGT, ACE, or AT(1)R mRNA. In summary, reduced responses of intrarenal tubular renin, ACE, and the AT(1)R protein to the stimulatory effects of chronic ANG II infusions, in the presence of ACEi, are associated with the effects of this treatment to ameliorate augmentations in blood pressure and intrarenal ANG II content during ANG II-induced hypertension.
机译：血管紧张素转换酶（ACE）抑制（ACEi）改善了注入ANG II的小鼠的高血压和肾内ANG II增强的发展。为了确定这些作用是否与小鼠肾内肾素-血管紧张素系统的变化有关，血管紧张素原（AGT），肾素，ACE，血管紧张素1型受体（AT（1）R）mRNA的表达（通过定量RT-PCR）和蛋白质[通过蛋白质印迹（WB）和/或免疫组化（IHC）]被分析。将C57BL / 6J雄性小鼠（9-12周龄）分配为对照组（n = 10），注入ANG II（ANG II = 8，400 ng x kg（-1）x min（-1）持续12天），仅使用ACEi（ACEi = 10，赖诺普利，100 mg / l），并注入ANG II + ACEi（ANG II + ACEi = 11）。与对照组（1.00）相比，ANG II使AGT蛋白（WB）增加（1.29 +/- 0.13，P <0.05），而ACEi（ACEi + ANG II，1.31 +/- 0.14 P <0.05）。 ACE II（通过WB）使ACE蛋白增加（1.21 +/- 0.08，P <0.05），单独使用ACEi（0.88 +/- 0.07，P <0.05）或与ANG II（0.80 + /-0.07，P <0.05）。 ANG II（1.27 +/- 0.06，P <0.05）和ACEi（1.17 +/- 0.06，P <0.05）增加了AT（1）R蛋白（通过WB），但ANG II + ACEi没有增加（1.15 +/- 0.06，不显着（NS）]。血管紧张素II（IHC半定量）增加了ANG II（1.49 +/- 0.23，P <0.05）和ACEi（1.57 +/- 0.15，P <0.05），但ANG II + ACEi（1.10 +/- 0.15）没有增加，NS）。在AGT，ACE或AT（1）R mRNA中未观察到明显变化。总之，在存在ACEi的情况下，肾小管肾素，ACE和AT（1）R蛋白对慢性ANG II输注的刺激作用的反应减少，与这种治疗改善血压升高的作用有关和在ANG II诱发的高血压期间的肾内ANG II含量。

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