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From the Department of Physiology, Eastern Virginia Medical School,
Norfolk, Va.
Correspondence to Russell L. Prewitt, PhD, Department of Physiology, Eastern Virginia Medical School, PO Box 1980, Norfolk, VA 23501. E-mail RLP{at}BORG.EVMS.EDU
AbstractAngiotensin II
(Ang II) may induce arterial hypertrophy either
directly or through an increase in arterial pressure. To
separate these 2 mechanisms, rats were implanted with osmopumps
delivering either Ang II (100 ng · kg-1 ·
min-1) or saline. 5-Bromo-2'-deoxyuridine (BrdU) was
delivered to both groups by osmopump (2.5 µg ·
kg-1 · min-1). Half of the rats in
each group were given minoxidil (9 mg · kg-1
· d-1) in their drinking water. After 14 days,
systolic blood pressure was 117±2, 124±3, and 115±2
mm Hg in the control, Ang IIminoxidil, and minoxidil groups,
respectively, and 181±6 mm Hg in the Ang II group
(P<0.05). After perfusion-fixation, the thoracic aorta,
carotid artery, small mesenteric artery, external spermatic artery, and
kidneys were harvested, paraffin-embedded, and used for morphological
measurements, immunohistochemistry for BrdU, and in situ hybridization
with a 35S-labeled riboprobe for platelet-derived
growth factorA chain (PDGF-A) mRNA. The walls of the aorta and
carotid arteries hypertrophied in the Ang II group only. There were no
significant morphological differences in the small arteries. BrdU was
negative in all arteries but positive in the renal tubules. Expression
of PDGF-A was elevated 8-fold in the thoracic aorta of the Ang II group
(P<0.05). These results show that (1)
arterial hypertrophy from Ang II infusion
occurs in response to elevated arterial pressure, (2)
hypertrophy was not associated with hyperplasia or
polyploidy of vascular smooth muscle cells, and (3) PDGF-A expression
correlated with elevated pressure and arterial wall
hypertrophy.
© 1998 American Heart Association, Inc.
Scientific Contributions
Pressure Mediates Angiotensin IIInduced Arterial Hypertrophy and PDGF-A Expression
Key Words: pressure angiotensin II hypertrophy growth substances
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