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Chronic Angiotensin II cardiovascular effects are inversely related to α1D‐adrenoceptors expression in aorta of adult Wistar rat
Author(s) -
Gallardo Ortiz Itzell Alejandrina,
IBARRA MAXIMILIANO,
LOPEZSANCHEZ PEDRO,
VILLALOBOSMOLINA RAFAEL
Publication year - 2009
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.23.1_supplement.933.3
Subject(s) - medicine , phenylephrine , endocrinology , angiotensin ii , blood pressure , aorta , muscle hypertrophy , contraction (grammar) , renin–angiotensin system , western blot , chemistry , biochemistry , gene
Angiotensin II plays an important role in regulating blood pressure, it provokes cardiovascular remodeling and hypertension, as well as an increase in α1‐adrenoceptors mRNA and protein. In the cardiovascular system α1‐adrenoceptors regulate processes like cardiac and arterial smooth muscle contraction and they have been implicated in pathological processes. We explored the in vivo Ang II continuous effect on α1‐adrenoceptors function and expression in aorta of Wistar rats. Osmotic minipumps filled with Ang II (200 ng/kg/min/day) were subcutaneously implanted in male Wistar rats. Blood pressure was measured and after 2 weeks aorta was isolated for contractile experiments. α1‐Adrenoceptors mRNA expression and protein were measured. Ang II increased blood pressure. Phenylephrine‐induced contraction in aorta was greater (Emax, 4.2g) in Ang II‐treated rats than in controls (2.7g). PCR and Western Blot data showed that α1B,1A‐adrenoceptors did not change with Ang II while α1D‐adrenoceptors were lower. Histological data showed hypertrophy in aortas with Ang II. The data suggest a crosstalk between Ang II and α1‐adrenergic pathways, nevertheless this effect seems not related with hypertension and hypertrophy induced by Ang II.

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