TY - JOUR
T1 - Role of α1D-adrenoceptors in vascular wall hypertrophy during angiotensin II-induced hypertension
AU - Gallardo-Ortíz, I. A.
AU - Rodríguez-Hernández, S. N.
AU - López-Guerrero, J. J.
AU - Del Valle-Mondragón, L.
AU - López-Sánchez, P.
AU - Touyz, R. M.
AU - Villalobos-Molina, R.
N1 - Publisher Copyright:
© 2016 John Wiley & Sons Ltd.
PY - 2016/4/1
Y1 - 2016/4/1
N2 - The invivo effect of continuous angiotensin II (Ang II) infusion on arterial blood pressure, vascular hypertrophy and α1-adrenoceptors (α1-ARs) expression was explored. Alzet® minipumps filled with Ang II (200ngkg-1min-1) were subcutaneously implanted in male Wistar rats (3months-old). Groups of rats were also treated with losartan, an AT1R antagonist, or with BMY 7378, a selective α1D-AR antagonist. Blood pressure was measured by tail-cuff; after 2 or 4weeks of treatment, vessels were isolated for functional and structural analyses. Angiotensin II increased systolic blood pressure. Phenylephrine-induced contraction in aorta was greater (40% higher) in Ang II-treated rats than in the controls, and similar effect occurred with KCl 80mm. Responses in tail arteries were not significantly different among the different groups. Angiotensin II decreased α1D-ARs without modifying the other α1-ARs and induced an increase in media thickness (hypertrophy) in aorta, while no structural change occurred in tail artery. Losartan prevented and reversed hypertension and hypertrophy, while BMY 7378 prevented and reversed the aorta's hypertrophic response, without preventing or reversing hypertension. Findings indicate that Ang II-induced aortic hypertrophic response involves Ang II-AT1Rs and α1D-ARs. Angiotensin II-induced α1D-AR-mediated vascular remodeling occurs independently of hypertension. Findings identify a α1D-AR-mediated process whereby Ang II influences aortic hypertrophy independently of blood pressure elevation.
AB - The invivo effect of continuous angiotensin II (Ang II) infusion on arterial blood pressure, vascular hypertrophy and α1-adrenoceptors (α1-ARs) expression was explored. Alzet® minipumps filled with Ang II (200ngkg-1min-1) were subcutaneously implanted in male Wistar rats (3months-old). Groups of rats were also treated with losartan, an AT1R antagonist, or with BMY 7378, a selective α1D-AR antagonist. Blood pressure was measured by tail-cuff; after 2 or 4weeks of treatment, vessels were isolated for functional and structural analyses. Angiotensin II increased systolic blood pressure. Phenylephrine-induced contraction in aorta was greater (40% higher) in Ang II-treated rats than in the controls, and similar effect occurred with KCl 80mm. Responses in tail arteries were not significantly different among the different groups. Angiotensin II decreased α1D-ARs without modifying the other α1-ARs and induced an increase in media thickness (hypertrophy) in aorta, while no structural change occurred in tail artery. Losartan prevented and reversed hypertension and hypertrophy, while BMY 7378 prevented and reversed the aorta's hypertrophic response, without preventing or reversing hypertension. Findings indicate that Ang II-induced aortic hypertrophic response involves Ang II-AT1Rs and α1D-ARs. Angiotensin II-induced α1D-AR-mediated vascular remodeling occurs independently of hypertension. Findings identify a α1D-AR-mediated process whereby Ang II influences aortic hypertrophy independently of blood pressure elevation.
KW - Alpha1D-adrenoceptors
KW - Angiotensin II
KW - Aorta
KW - High blood pressure
KW - Hypertrophy
UR - http://www.scopus.com/inward/record.url?scp=84963542368&partnerID=8YFLogxK
U2 - 10.1111/aap.12035
DO - 10.1111/aap.12035
M3 - Artículo
C2 - 26845248
SN - 1474-8665
VL - 35
SP - 17
EP - 31
JO - Autonomic and Autacoid Pharmacology
JF - Autonomic and Autacoid Pharmacology
IS - 3
ER -