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Submitted on April 17, 2002
Accepted on May 1, 2002
From the Departments of Medicine (S.P.B., L.S.L., Z.L.), Comparative Medicine (B.E.O.), and Pathology (C.L.C.), Oregon Health and Science University and Portland VA Medical Center, Portland, Ore, and the Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology (R.C.S.), College of Veterinary Medicine, Washington State University, Pullman.
* To whom correspondence should be addressed. E-mail: bagbys{at}ohsu.edu.
ObjectiveTo identify vascular cells capable of responding to angiotensin II (Ang II) generated in conduit arteries, we examined the Ang II type 1 receptor (AT1R) and Ang II type 2 receptor (AT2R) in the thoracic aorta (TA) and abdominal aorta (AA) and branches in 90-day fetal, 3-week postnatal, and 6-month adult microswine.
Methods and ResultsBy
autoradiography
(125I-[Sar1Ile8]-Ang
II with or without AT1R- or AT2R-selective analogues or
125I-CGP
42112), there were striking rostrocaudal differences in (1) AT2R
binding at all ages (prominent in AA wall and branches, sparse in TA
wall and branches) and (2) a non-AT2R binding site for CGP 42112
(consistently evident in postnatal TA and branches but absent
in AA and branches). Furthermore, patterns of AT2R distribution in
infradiaphragmatic arteries were developmentally distinct. In fetal
AAs, high-density AT2Rs occupied the inner 60% of the
medial-endothelial wall. In postnatal AAs, AT2Rs were
sparse in the medial-endothelial wall but prominent in
a circumferential smooth muscle
-actin--negative cell layer at the
medial-adventitial border, occupying
20% to 25% of the AA
cross-sectional area. AT1R density in the TA and AA
medial-endothelial wall increased with age, whereas
AT2R density decreased after birth.
ConclusionsA novel AT2R-positive cell layer confined to postnatal infradiaphragmatic arteries physically links adventitial and medial layers, appears optimally positioned to transduce AT2R-dependent functions of local Ang II, and suggests that adventitial Ang II may elicit regionally distinct vascular responses.
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