血管收缩
缓激肽
血管紧张素II
内分泌学
内科学
受体
刺激
化学
缬沙坦
对抗
主动脉
肾素-血管紧张素系统
血管舒张
封锁
血管紧张素受体
收缩(语法)
药理学
兴奋剂
肽类激素
收缩性
医学
血管紧张素Ⅱ受体1型
内皮
血管紧张素1
作者
Jazmin Flores-Monroy,Ignacio Valencia-Hernandez,Luis Alfredo Rocha-Ceron,Diana Ramirez-Hernandez,Diego Lezama-Martinez
标识
DOI:10.1177/14703203261422141
摘要
Introduction The study of the receptors of the renin-angiotensin and kinin-kallikrein systems and their interactions has enhanced our understanding of hypertension physiology and contributed to the development of improved pharmacological treatments (McCarthy et al. 2025). Objective This work aimed to investigate the functional interactions among AT1, AT2, and B2 receptors specifically the effects of agonist-agonist, agonist-antagonist, and antagonist-antagonist combinations on vasocontractile response to Ang II. Methods Concentration-response curves to Ang II were performed in WKY and SHR rat aortic rings in the presence of bradykinin (BK), valsartan, CGP42112A, HOE140, and their combinations. NO levels were indirectly determinated by the Griess reaction in aortic rings. Results Ang II induced a stronger contractile response in SHR compared with WKY. AT1R antagonism and AT2R receptor stimulation significantly reduced vasoconstriction and increased NO levels. BK also attenuated the contractile response without increasing NO levels. In contrast, blockade of B2R or AT2R did not reduce maximal contraction. Combined treatments involving valsartan or CGP42112A decreased Ang II reactivity. Conclusion Activation of AT2R and B2R counteracts Ang II–induced vasoconstriction through NO-dependent and NO-independent mechanisms. Receptor heterodimerization appears to contribute to these modulatory effects.
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