Key result
Angiotensin 1-7 ameliorates Angiotensin II-stimulated endoplasmic reticulum stress to raise nitric oxide bioavailability and preserve endothelial function via the Mas receptor.
p-value: p=<0.05
Angiotensin 1-7 protects against Angiotensin II-induced endothelial dysfunction by ameliorating endoplasmic reticulum stress and preserving nitric oxide bioavailability via the Mas receptor.
Supports Ang 1-7 counter-regulation of Ang II in endothelium; hypothesis-generating for vascular therapies pending in vivo validation.
Angiotensin 1-7 (Ang 1-7) counter-regulates the cardiovascular actions of angiotensin II (Ang II). The present study investigated the protective effect of Ang 1-7 against Ang II-induced endoplasmic reticulum (ER) stress and endothelial dysfunction. Ex vivo treatment with Ang II (0.5 μM, 24 hours) impaired endothelium-dependent relaxation in mouse aortas; this harmful effect of Ang II was reversed by co-treatment with ER stress inhibitors, l4-phenylbutyric acid (PBA) and tauroursodeoxycholic acid (TUDCA) as well as Ang 1-7. The Mas receptor antagonist, A779, antagonized the effect of Ang 1-7. The elevated mRNA expression of CHOP, Grp78 and ATF4 or protein expression of p-eIF2α and ATF6 (ER stress markers) in Ang II-treated human umbilical vein endothelial cells (HUVECs) and mouse aortas were blunted by co-treatment with Ang 1-7 and the latter effect was reversed by A779. Furthermore, Ang II-induced reduction in both eNOS phosphorylation and NO production was inhibited by Ang 1-7. In addition, Ang 1-7 decreased the levels of ER stress markers and augmented NO production in HUVECs treated with ER stress inducer, tunicamycin. The present study provides new evidence for functional antagonism between the two arms of the renin-angiotensin system in endothelial cells by demonstrating that Ang 1-7 ameliorates Ang II-stimulated ER stress to raise NO bioavailability, and subsequently preserves endothelial function.
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Murugan et al. (2015) studied Angiotensin II-induced endoplasmic reticulum stress and endothelial dysfunction. Angiotensin 1-7 vs. Angiotensin II alone was evaluated on Endothelium-dependent relaxation and expression of ER stress markers (p=<0.05). Angiotensin 1-7 ameliorates Angiotensin II-stimulated endoplasmic reticulum stress to raise nitric oxide bioavailability and preserve endothelial function via the Mas receptor.
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