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Angiotensin II modulates vascular smooth muscle cells alpha‐1D‐adrenoceptors
Author(s) -
GallardoOrtíz Itzell,
Barajas Maximiliano Ibarra,
LópezSánchez Pedro,
VillalobosMolina Rafael
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.829.3
Subject(s) - angiotensin ii , losartan , medicine , endocrinology , vascular smooth muscle , angiotensin ii receptor type 1 , alpha (finance) , stimulation , receptor , muscle hypertrophy , renin–angiotensin system , smooth muscle , chemistry , biology , blood pressure , construct validity , patient satisfaction , nursing
Angiotensin II plays an important role in regulating systemic arterial pressure, provokes cardiovascular remodelling and hypertension, as well as an increase in alpha1‐adrenoceptors mRNA and protein. The aim of this work was evaluate the influence of angiotensin II on alpha 1D‐adrenoceptors in isolated smooth muscle cells of Wistar rat aorta. Smooth muscle cells were incubated with angiotensin II (100 nM) for different periods of time (30min–24hrs), and then protein by Westernblot was determined for the alpha 1‐adrenoceptor subtype. The results show an important increment of alpha 1D‐adrenoceptors at 30 min by angiotensin II action, then a time‐dependent diminution in expression of protein at later measurement points. The maximal expression was blocked by losartan and ciclohexymide. This data suggesting that stimulation of AT1 receptors by angiotensin II in isolated cells conduce to increase of alpha 1D‐adrenoceptors and this effect is due to synthesis the novo of alpha 1D‐adrenoceptors, however there is not correlation with longer exposure of animals to the peptide, i.e., hypertension and hypertrophy, and suggest compensatory mechanisms in the animals not observed in isolated cells. Supported by Conacyt 47481, PAPIIT IN203205 and Fundación Miguel Alemán