| Involvement of oxidative stress in the profibrotic action of aldosterone. Interaction wtih the renin-angiotension system. | |
| | |
MedLine Citation:
|
PMID: 15243979 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
BACKGROUND: The aim of this study was to investigate the involvement of angiotensin II and oxidative stress on cardiovascular damage induced by chronic subcutaneous aldosterone infusion in the absence of salt loading. METHODS: Sprague-Dawley rats were infused with d-aldosterone (0.75 microg/h subcutaneously) for 6 weeks. Blood pressure was measured with the tail-cuff method. Small arteries were investigated on a pressurized myograph. Cardiovascular and renal collagen was evaluated by Sirius red staining. Systemic oxidant excess was measured with plasma 8-isoprostane by ELISA and by measurement of thiobarbituric acid-reactive substances. Vascular reactive oxygen species were studied using hydroethidine and NADPH-generated superoxide anion measured by lucigenin chemiluminescence. RESULTS: After 6 weeks of treatment, systolic blood pressure was significantly increased in aldosterone-infused rats (170+/-8 v 123+/-2 mm Hg in controls, P < .05). Progression of hypertension was partially prevented by co-administration of losartan (AT1 receptor blocker) or tempol (superoxide dismutase mimetic): 140+/-4 and 149+/-6 mm Hg, respectively, P < .05 versus the aldosterone group. Aldosterone induced renal but not cardiac hypertrophy, which was not prevented by losartan or by tempol. Moreover, losartan and tempol failed to prevent vascular hypertrophy of resistance mesenteric vessels. However, losartan (0.77%+/-0.05%) and tempol (0.65%+/-0.10%) prevented cardiac fibrosis in the midmyocardium in the aldosterone group (1.03%+/-0.12% v 0.68%+/-0.07% positive staining per area in control, P < .05). In the kidney, collagen accumulation of aldosterone-infused rats was also significantly decreased by losartan (-77%) and tempol (-60%). Similar effects were obtained on aortic fibrosis. Aldosterone increased serum 8-isoprostane levels.This increase was blunted by losartan and tempol. Losartan and tempol totally prevented vascular, cardiac, and renal increase of NADPH-induced superoxide production stimulated by aldosterone. CONCLUSIONS: Our data suggest that the profibrotic but not the hypertrophic action of aldosterone are mediated at least in part by reactive oxygen species generation and involve an interaction with the renin-angiotensin system. |
| | |
Authors:
|
Marc Iglarz; Rhian M Touyz; Emilie C Viel; Farhad Amiri; Ernesto L Schiffrin |
Related Documents
:
|
209529 - Deviation of plasmatic aldosterone and significance of the stimulating (acth-cortrosyn)... 2990769 - Plasma na+-k+ atpase inhibitory activity in normal and hypertensive subjects: relations... 18212439 - Effect of age on hypertension: analysis of over 4,800 referred hypertensive patients. 2561139 - Brain corticosteroid receptors and regulation of arterial blood pressure. 2527199 - Low dose atrial natriuretic factor in primary aldosteronism: renal, hemodynamic, and va... 9928749 - Impaired baroreflex function and arterial compliance in primary aldosteronism. 8535549 - Independent association between fasting plasma insulin and ambulatory blood pressure in... 6310949 - Vasopressin, acth and neonatal haemodynamics. 20164739 - Validation of the andon kd-575 automated blood pressure monitor according to the europe... |
Publication Detail:
|
Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: American journal of hypertension Volume: 17 ISSN: 0895-7061 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2004 Jul |
Date Detail:
|
Created Date: 2004-07-09 Completed Date: 2004-11-06 Revised Date: 2009-02-24 |
Medline Journal Info:
|
Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
|
Languages: eng Pagination: 597-603 Citation Subset: IM |
Affiliation:
|
Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Aldosterone
/
administration & dosage* Animals Antihypertensive Agents / administration & dosage Antioxidants / administration & dosage Biological Markers / blood Blood Pressure / drug effects Cyclic N-Oxides / administration & dosage Disease Models, Animal Endocardium / drug effects, pathology Endothelium, Vascular / drug effects, metabolism, physiopathology Fibrosis Infusions, Intra-Arterial Kidney / drug effects, pathology Losartan / administration & dosage Male Models, Cardiovascular NADP / drug effects, metabolism Nitroprusside / administration & dosage Oxidative Stress / drug effects* Pericardium / drug effects, pathology Rats Rats, Sprague-Dawley Reactive Oxygen Species / metabolism Renin-Angiotensin System / drug effects* Spin Labels Systole / drug effects Thiobarbituric Acid Reactive Substances / metabolism Vasodilator Agents / administration & dosage |
| Chemical | |
Reg. No./Substance:
|
0/Antihypertensive Agents; 0/Antioxidants; 0/Biological Markers; 0/Cyclic N-Oxides; 0/Reactive Oxygen Species; 0/Spin Labels; 0/Thiobarbituric Acid Reactive Substances; 0/Vasodilator Agents; 114798-26-4/Losartan; 15078-28-1/Nitroprusside; 2226-96-2/tempol; 52-39-1/Aldosterone; 53-59-8/NADP |
| Comments/Corrections | |
Comment In:
|
Am J Hypertens. 2005 Mar;18(3):441
[PMID:
15797667
]
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Physiology: does gut hormone PYY3-36 decrease food intake in rodents?
Next Document: Fatal presentation of ornithine transcarbamylase deficiency in a 62-year-old man and family studies.