Author(s)

Itzell Alejandrina Gallardo-Ortíz^1,2*, Juan Pablo de Jesús Benítez-Garrido³, Santiago C. Sigrist-Flores⁴, Juan Javier López-Guerrero³, Enrique Hong³, Rafael Villalobos-Molina^1,2*

¹Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.
²Carrera de Enfermería, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.
³Departamento de Farmacobiología, Centro de Investigación and de Estudios Avanzados-IPN, Ciudad de México, México.
⁴Carrera de Médico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, México.

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 (α_1A-AR antagonist), AH11110A (α_1B-AR antagonist), or BMY-7378 (α_1D-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. α_1D-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. α_1D-AR increased at 30 and 60 min post Ang II exposure, the α_1A-AR diminished from 1 to 4 h, while α_1B-AR remained unchanged over 24 h of Ang II exposure. Ang II induced an increase of α_1D-AR at short times, and BMY-7378 protected α_1D-AR from desensitization.

Angiotensin II, α_1D-AR, α₁-AR Expression, Rat aorta, Smooth Muscle Cells

Gallardo-Ortíz, I. , Benítez-Garrido, J. , Sigrist-Flores, S. , López-Guerrero, J. , Hong, E. and Villalobos-Molina, R. (2024) Influence of Angiotensin II on α₁-Adrenergic Receptors Function in Rat Aorta and Expression in Vascular Smooth Muscle Cells. Journal of Biosciences and Medicines, 12, 123-134. doi: 10.4236/jbm.2024.124011.