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Angiotensin II increases blood pressure and functional expression of alpha1D‐adrenoceptors in aorta of adult Wistar rat
Author(s) -
GallardoOrtiz Itzell A.,
LopezGuerrero J. Javier,
Ibarra Maximiliano,
VillalobosMolina Rafael
Publication year - 2006
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.20.5.a982-a
Subject(s) - phenylephrine , medicine , aorta , blood pressure , endocrinology , contraction (grammar) , angiotensin ii , renin–angiotensin system , chemistry
Angiotensin II (Ang II) plays an important role in regulating systemic arterial pressure. Interestingly, it is known that RAS components are enhanced in young SHR (plasma renin activity and angiotensinogen concentration); these components might contribute to pathogenesis of genetic hypertension. In the cardiovascular system α1‐adrenoceptors regulate processes like cardiac and arterial smooth muscle contraction and they have been implicated in pathological processes such as cardiac hypertrophy or ischemia‐induced cardiac arrythmias. The aim of this work was to explore the in vivo Ang II continuous effect on α 1D − adrenoceptors functional expression in aorta of Wistar rats. Osmotic minipumps (Alzet) filled with Ang II (release of 200 ng/kg/min/14 days) were subcutaneously implanted in male Wistar rats of 3 months of age. Arterial blood pressure was measured by a tail‐cuff method; after 2 weeks aorta was isolated and used for contractile experiments. Ang II induced an early increase in blood pressure and a maximal effect at 10 days (178 ± 10 vs 110 ± 5 mmHg). Phenylephrine‐induced contraction in aorta was greater (4.2 ± 0.3 g maximal effect) in Ang II‐treated rats than in controls (2.7 ± 0.4 g). The data suggest that Ang II‐induced hypertension might be mediated by α 1D − adrenoceptors augmented expression. It will be very interesting to determine the mRNA and protein of α 1D − adrenoceptors in aorta of Ang II treated rats. Supported in part by grants 47481 from Conacyt (RV‐M) and PAPIIT IN210702 (MI).