Exaggerated vasomotor response to ANG II in rats with fetal programming of hypertension associated with exposure to a low-protein diet during gestation.

Details

Serval ID
serval:BIB_99832716EDFB
Type
Article: article from journal or magazin.
Collection
Publications
Title
Exaggerated vasomotor response to ANG II in rats with fetal programming of hypertension associated with exposure to a low-protein diet during gestation.
Journal
American journal of physiology. Regulatory, integrative and comparative physiology
Author(s)
Yzydorczyk C., Gobeil F., Cambonie G., Lahaie I.,  N.L., Samarani S., Ahmad A., Lavoie J.C., Oligny L.L., Pladys P., Hardy P., Nuyt A.M.
ISSN
0363-6119 (Print)
ISSN-L
0363-6119
Publication state
Published
Issued date
10/2006
Peer-reviewed
Oui
Volume
291
Number
4
Pages
R1060-8
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
The renin-angiotensin system plays a key role in the initiation and maintenance of elevated blood pressure associated with altered intrauterine milieu. The current studies were undertaken to verify whether vascular response to ANG II is increased in adult offspring of low-protein fed dams (LP) compared with control (CTRL) and if so, to examine underlying mechanism(s). ANG II-induced contraction of carotid rings was increased in LP (E(max), the maximum asymptote of the curve, relative to maximal response to KCl 80 mM: 230 +/- 3% LP vs. 201 +/- 2% CTRL, P < 0.05). In both groups, contraction to ANG II was mediated solely by AT1R. Responses to thromboxane A2 analog U-46619 and to KCl 80 mM under step increases in tension were similar between groups. Endothelium depletion enhanced contraction to ANG II in both groups, more so in LP. Blockade of endothelin formation had no effect on response to ANG II, and ANG-(1-7) did not elicit vasomotor response in either group. Superoxide dismutase (SOD) analog Tempol normalized LP without modifying CTRL response to ANG II. Basal levels of superoxide (aortic segments, lucigenin-enhanced chemiluminescence and fluorescent dye hydroethidine) were higher in LP. ANG II further increased superoxide production in LP only, and this was inhibited by coincubation with diphenylene iodonium or apocynin (inhibitor of NADPH oxidase complex). AT1R expression in carotid arteries was increased in LP, whereas SOD expression was unchanged. In conclusion, vasoconstriction to ANG II is exaggerated in this model of developmental programming of hypertension, secondary to enhanced vascular production of superoxide anion by NADPH oxidase with concomitant increase of AT1R expression.
Keywords
Age Factors, Angiotensin II/pharmacology, Animal Feed, Animals, Antioxidants/pharmacology, Blotting, Western, Cyclic N-Oxides/pharmacology, Diet, Protein-Restricted, Dietary Proteins/pharmacology, Endothelium, Vascular/drug effects, Endothelium, Vascular/physiology, Female, Hypertension/physiopathology, Male, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Wistar, Reactive Oxygen Species/metabolism, Receptor, Angiotensin, Type 1/metabolism, Spin Labels, Superoxide Dismutase/metabolism, Vasoconstriction/drug effects, Vasoconstriction/physiology, Vasoconstrictor Agents/pharmacology
Pubmed
Web of science
Create date
21/11/2019 16:08
Last modification date
22/11/2019 6:26
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