Effects of Angiotensin-(1-7) and Angiotensin II on Acetylcholine-Induced Vascular Relaxation in Spontaneously Hypertensive Rats
Effects of Angiotensin-(1-7) and Angiotensin II on Acetylcholine-Induced Vascular Relaxation in Spontaneously Hypertensive Rats
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血管紧张素-(1-7) 和血管紧张素 II 对乙酰胆碱诱导的自发性高血压大鼠血管舒张的影响
DOI：
10.1155/2019/6512485
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发表时间：
2019-11
影响因子：
--
通讯作者：
Han Ying
中科院分区：
文献类型：
--
作者：
Zhang Feng;Xu Yu;Pan Yan;Sun Shuo;Chen Aidong;Li Peng;Bao Changlei;Wang Jian;Tang Haiyang;Han Ying
Endothelial dysfunction of small arteries occurs in patients with hypertension and in various hypertensive models. Endothelial function is usually evaluated by the degree of acetylcholine- (ACh-) induced vascular relaxation. Our previous study has found that compared to Wistar-Kyoto rats (WKY), ACh-induced vasodilatation was attenuated significantly in the mesenteric artery (MA), coronary artery (CA), and pulmonary artery (PA) of spontaneously hypertensive rats (SHR). This study investigated the influence of angiotensin- (Ang-) (1-7) and Ang II on blood pressure and ACh-induced vascular relaxation, as well as their interactive roles and downstream signal pathways in SHR and WKY. Intravenous injection of Ang II significantly increased, while Ang-(1-7) decreased the mean arterial pressure (MAP) in SHR. Ang-(1-7) improved ACh-induced relaxation in the MA, CA, and PA of SHR, while Ang II further attenuated it, which were inhibited by pretreatment with Mas receptor antagonist A-779 or AT1 receptor antagonist losartan, respectively. Ang-(1-7) decreased the basal arterial tension, and Ang II induced great vasoconstriction in SHR. Pretreatment with Ang-(1-7) inhibited the Ang II-induced pressor response, vasoconstriction, and the effects on ACh-induced relaxation in SHR. AT1 receptor expression was higher, while nitric oxide (NO), cGMP, and protein kinase G (PKG) levels of arteries were lower in SHR than in WKY. Ang II decreased, while Ang-(1-7) increased, the levels of NO, cGMP, and PKG of arteries. In addition, pretreatment with Ang-(1-7) inhibited the Ang II-induced reduction of NO, cGMP, and PKG in SHR. These results indicate that the activation of the Mas receptor by Ang-(1-7) can improve endothelial function and decrease MAP in SHR and inhibit the deteriorative effect of Ang II on endothelial function through the NO-cGMP-PKG pathway.
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血管紧张素-(1-7) 抑制近端肾小管细胞中血管紧张素 II 刺激的 MAP 激酶磷酸化
影响因子：
19.6
作者：
Su, Z.;Zimpelmann, J.;Burns, K. D.
通讯作者：
Burns, K. D.
影响因子：
3
作者：
Yousif MHM;Benter IF;Diz DI;Chappell MC
通讯作者：
Chappell MC
肾素-血管紧张素系统的 ACE2/血管紧张素 1-7 轴在心力衰竭中的作用。
影响因子：
20.1
作者：
Patel VB;Zhong JC;Grant MB;Oudit GY
通讯作者：
Oudit GY
影响因子：
1.9
作者：
Durik M;van Veghel R;Kuipers A;Rink R;Haas Jimoh Akanbi M;Moll G;Danser AH;Roks AJ
通讯作者：
Roks AJ
影响因子：
8.3
作者：
Kerr, S;Brosnan, MJ;Hamilton, CA
通讯作者：
Hamilton, CA