Influence of Angiotensin II on α<sub>1</sub>-Adrenergic Receptors Function in Rat Aorta and Expression in Vascular Smooth Muscle Cells
Influence of Angiotensin II on α<sub>1</sub>-Adrenergic Receptors Function in Rat Aorta and Expression in Vascular Smooth Muscle Cells作者机构：Unidad de Biomedicina Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de México Tlalnepantla México Carrera de Enfermería Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de México Tlalnepantla México Departamento de Farmacobiología Centro de Investigación and de Estudios Avanzados-IPN Ciudad de México México Carrera de Médico Cirujano Facultad de Estudios Superiores Iztacala Universidad Nacional Autónoma de México Tlalnepantla México
出 版 物：《Journal of Biosciences and Medicines》 (生物科学与医学（英文）)
年 卷 期：2024年第12卷第4期
页 面：123-134页
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
主 题：Angiotensin II α1D-AR α1-AR Expression Rat aorta Smooth Muscle Cells
摘 要：Angiotensin II (Ang II) is the main mediator of the Renin-Angiotensin-System acting on AT1 and other AT receptors. It is regarded as a pleiotropic agent that induces many actions, including functioning as a growth factor, and as a contractile hormone, among others. The aim of this work was to examine the impact of Ang II on the expression and function of α1-adrenergic receptors (α1-ARs) in cultured rat aorta, and aorta-derived smooth muscle cells. Isolated Wistar rat aorta was incubated for 24 h in DMEM at 37˚C, then subjected to isometric tension and to the action of added norepinephrine, in concentration-response curves. Ang II was added (1 × 10−5 M), and in some experiments, 5-Methylurapidil (α1A-AR antagonist), AH11110A (α1B-AR antagonist), or BMY-7378 (α1D-AR antagonist), were used to identify the α1-AR involved in the response. Desensitization of the contractile response to norepinephrine was observed due to incubation time, and by the Ang II action. α1D-AR was protected from desensitization by BMY-7378;while RS-100329 and prazosin partially mitigated desensitization. In another set of experiments, isolated aorta-derived smooth muscle cells were exposed to Ang II and α1-ARs proteins were evaluated. α1D-AR increased at 30 and 60 min post Ang II exposure, the α1A-AR diminished from 1 to 4 h, while α1B-AR remained unchanged over 24 h of Ang II exposure. Ang II induced an increase of α1D-AR at short times, and BMY-7378 protected α1D-AR from desensitization.
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