| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2003;41:50.)
© 2003 American Heart Association, Inc.
Scientific Contributions |
From the Departments of Pathology (G.L.B.) and Internal Medicine (C.D.S., F.M.F.), University of Iowa College of Medicine and Cardiovascular Center, Iowa City, Iowa.
Correspondence to Gary L. Baumbach, MD, Department of Pathology, 105 Medical Laboratories, University of Iowa College of Medicine, Iowa City, IA 52242. E-mail g-baumbach{at}uiowa.edu
We examined the hypothesis that the renin-angiotensin system plays an important role in vascular remodeling (defined as reduced external diameter) during chronic hypertension. We measured pressure, diameter, and cross-sectional area of the vessel wall in maximally dilated cerebral arterioles in transgenic mice that overexpress both human renin and human angiotensinogen and in spontaneously hypertensive mice, a model of chronic hypertension that is thought to develop independently of the renin-angiotensin system. Systemic arterial pressure under conscious conditions was increased by similar amounts in transgenically hypertensive mice (153±6 versus 117±4 mm Hg in controls; mean±SE, P<0.05) and spontaneously hypertensive mice (148±5 versus 112±5 mm Hg; P<0.05). The external diameter of maximally dilated cerebral arterioles was reduced in transgenically hypertensive mice (52±2 versus 66±3 µm; P<0.05), but not in spontaneously hypertensive mice (58±4 versus 60±4 µm; P>0.05). The cross-sectional area of the vessel wall was increased in both transgenically hypertensive mice (504±53 versus 379±37 µm2; P<0.05) and spontaneously hypertensive mice (488±40 versus 328±38 µm2; P<0.05). During maximal dilatation, the stress-strain curves in cerebral arterioles of transgenically hypertensive mice and spontaneously hypertensive mice were shifted to the right of the curves in corresponding controls, an indication that arteriolar distensibility was increased in the transgenically and spontaneously hypertensive groups. Thus, cerebral arterioles undergo remodeling and hypertrophy in transgenically hypertensive mice, but only hypertrophy in spontaneously hypertensive mice. These findings support the hypothesis that the renin-angiotensin system is an important determinant of vascular remodeling during chronic hypertension.
Key Words: renin-angiotensin system mice vasculature remodeling hypertrophy hypertension, chronic
This article has been cited by other articles:
![]() |
F. M. Faraci Surviving the Remodel: The Impact of Hypertension During Pregnancy Hypertension, April 1, 2008; 51(4): 995 - 996. [Full Text] [PDF] |
||||
![]() |
A. M. Beyer, G. L. Baumbach, C. M. Halabi, M. L. Modrick, C. M. Lynch, T. D. Gerhold, S. M. Ghoneim, W. J. de Lange, H. L. Keen, Y.-S. Tsai, et al. Interference With PPAR{gamma} Signaling Causes Cerebral Vascular Dysfunction, Hypertrophy, and Remodeling Hypertension, April 1, 2008; 51(4): 867 - 871. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Girouard, L. Park, J. Anrather, P. Zhou, and C. Iadecola Cerebrovascular Nitrosative Stress Mediates Neurovascular and Endothelial Dysfunction Induced by Angiotensin II Arterioscler. Thromb. Vasc. Biol., February 1, 2007; 27(2): 303 - 309. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. H.J. Heerkens, A. S. Izzard, and A. M. Heagerty Integrins, Vascular Remodeling, and Hypertension Hypertension, January 1, 2007; 49(1): 1 - 4. [Full Text] [PDF] |
||||
![]() |
G. L. Baumbach, S. P. Didion, and F. M. Faraci Hypertrophy of Cerebral Arterioles in Mice Deficient in Expression of the Gene for CuZn Superoxide Dismutase Stroke, July 1, 2006; 37(7): 1850 - 1855. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Girouard, L. Park, J. Anrather, P. Zhou, and C. Iadecola Angiotensin II Attenuates Endothelium-Dependent Responses in the Cerebral Microcirculation Through Nox-2-Derived Radicals Arterioscler. Thromb. Vasc. Biol., April 1, 2006; 26(4): 826 - 832. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Sethi, S. Iida, C. D. Sigmund, and D. D. Heistad Renal Thrombotic Microangiopathy in a Genetic Model of Hypertension in Mice Experimental Biology and Medicine, February 1, 2006; 231(2): 196 - 203. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Kazama, J. Anrather, P. Zhou, H. Girouard, K. Frys, T. A. Milner, and C. Iadecola Angiotensin II Impairs Neurovascular Coupling in Neocortex Through NADPH Oxidase-Derived Radicals Circ. Res., November 12, 2004; 95(10): 1019 - 1026. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. L. Baumbach, C. D. Sigmund, and F. M. Faraci Structure of Cerebral Arterioles in Mice Deficient in Expression of the Gene for Endothelial Nitric Oxide Synthase Circ. Res., October 15, 2004; 95(8): 822 - 829. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. W. Stepp, D. M. Pollock, and J. C. Frisbee Low-flow vascular remodeling in the metabolic syndrome X Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H964 - H970. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. J. Ryan, S. P. Didion, S. Mathur, F. M. Faraci, and C. D. Sigmund PPAR{gamma} Agonist Rosiglitazone Improves Vascular Function and Lowers Blood Pressure in Hypertensive Transgenic Mice Hypertension, March 1, 2004; 43(3): 661 - 666. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Iadecola and P. B. Gorelick Hypertension, Angiotensin, and Stroke: Beyond Blood Pressure Stroke, February 1, 2004; 35(2): 348 - 350. [Full Text] [PDF] |
||||
![]() |
S. P. Didion and F. M. Faraci Angiotensin II Produces Superoxide-Mediated Impairment of Endothelial Function in Cerebral Arterioles Stroke, August 1, 2003; 34(8): 2038 - 2042. [Abstract] [Full Text] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |