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      Effects of Immobilization Stress on Kidneys of Wistar Male Rats: A Morphometrical and Stereological Analysis

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          Abstract

          This paper verifies the morphological changes induced by immobilization stress on the kidney of rats by using stereological methods. Fifteen 4-week-old Wistar male rats were randomly assigned to control (n = 7) and stressed (n = 8) groups. Stress stimuli were performed over 5 weeks by immobilization of the rats for 2 h daily in a rigid opaque plastic cylinder that restrained their movements. Increases in the adrenal mass index (p < 0.05) and decreases in serum testosterone levels (p < 0.05) demonstrated the efficacy of the stressor stimuli. Stressed rats presented diminished body weight gain when compared to controls (p < 0.05). The mean values of kidney weight, kidney volume, kidney volume index and glomerular volume density were significantly lower in the stressed group (p < 0.05); nevertheless, no significant difference was found in the cortical/medullar ratio or in the volume-weighted mean glomerular volume. The number of glomeruli per kidney was 45% lower in the stressed group (p < 0.0001), but no change in serum creatinine levels was found. However, the morphological alterations may have serious implications predisposing individuals to renal disease and hypertension in adult life.

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          The general adaptation syndrome and the diseases of adaptation.

          H Selye (1946)
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            Prenatal glucocorticoids and long-term programming.

            Epidemiological evidence suggests that low birth weight is associated with an increased risk of cardiovascular, metabolic and neuroendocrine disorders in adult life. Glucocorticoid administration during pregnancy reduces offspring birth weight and alters the maturation of the lung and other organs. We hypothesised that prenatal exposure to excess glucocorticoids or stress might represent a mechanism linking foetal growth with adult pathophysiology. In rats, birth weight is reduced following prenatal exposure to the synthetic steroid dexamethasone, which readily crosses the placenta, or to carbenoxolone, which inhibits 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the physiological feto-placental 'barrier' to maternal glucocorticoids. As adults, the offspring exhibit permanent hypertension, hyperglycaemic, increased hypothalamic-pituitary-adrenal (HPA) axis activity and behaviour reminiscent of anxiety. Physiological variations in placental 11beta-HSD2 activity correlate directly with foetal weight. In humans, 11beta-HSD2 gene mutations cause low birth weight. Moreover, low-birth-weight babies have higher plasma cortisol levels throughout adult life, indicating HPA axis programming. The molecular mechanisms may reflect permanent changes in the expression of specific transcription factors, key among which is the glucocorticoid receptor (GR) itself. The differential programming of the GR in different tissues reflects effects upon one or more of the multiple tissue-specific alternate first exons/promoters of the GR gene. Overall, the data suggest that both pharmacological and physiological exposure prenatally to excess glucocorticoids programmes cardiovascular, metabolic and neuroendocrine disorders in adult life.
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              The hypothalamic-pituitary-adrenal axis activity as a predictor of cardiovascular disease, type 2 diabetes and stroke.

              The hypothalamic-pituitary-adrenal (HPA) axis, the mediator of cortisol, plays a central role in the homeostatic processes. In this study, we addressed the potential impact of HPA axis activity on established anthropometric, metabolic and haemodynamic risk factors for cardiovascular disease (CVD), type 2 diabetes mellitus and stroke. A cross-sectional study. A subgroup of 284 men from a population sample of 1040 at the age of 51 years. Anthropometric measurements included body mass index (BMI, kg m-2), waist/hip circumference ratio (WHR) and abdominal sagittal diameter (D). Overnight fasting values of blood glucose, serum insulin, triglycerides, total, low (LDL) and high density (HDL) lipoprotein cholesterol, as well as resting heart rate and blood pressure, were also determined. By using repeated diurnal salivary cortisol measurements during everyday conditions, methods were developed to characterize the status of the HPA axis, and set in relation to the anthropometric, metabolic and haemodynamic measurements. In bivariate analyses, risk factors intercorrelated in clusters of anthropometric (BMI, WHR, D), metabolic (insulin, glucose and their ratio, triglycerides, cholesterol [total and LDL], HDL cholesterol [negative]) and haemodynamic (systolic and diastolic blood pressure and heart rate) measurements. This was also the case in the two-dimensional scaling analysis, where, however, HDL separated out. A normal HPA axis status, characterized by high variability and morning cortisol values, as well as a clear response to a standardized lunch and dexamethasone suppression test, was then introduced by a statistical weighting procedure. This did not essentially change the results of either the bivariate correlation matrix or the two-dimensional scaling analysis. A similar introduction of a pathological HPA axis, characterized by low variability and morning cortisol values, a poor lunch-induced cortisol response and a blunted dexamethasone suppression of cortisol, changed the results markedly. Now strong and consistent correlations were found not only within but also between different clusters of risk factors, which also congregated into one distinct cluster, again except for HDL cholesterol. These results disclose the prospect of an overriding function of a pathological HPA axis on other, established risk factors for CVD, type 2 diabetes and stroke. Its close association to HPA axis dysfunction may explain the previously reported powerful risk indication of abdominal obesity for the diseases mentioned. The HPA axis abnormality has been reported to be a characteristic consequence of frequently repeated or chronic environmental stress challenges.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2011
                November 2011
                28 June 2011
                : 34
                : 6
                : 424-429
                Affiliations
                aUrogenital Research Unit, IBRAG, Rio de Janeiro State University, and bDepartment of Applied Mathematics, IME, Rio de Janeiro State University, Rio de Janeiro, Brazil
                Author notes
                *Célia Martins Cortez, Department of Applied Mathematics, IME, Rio de Janeiro State University, Rua São Francisco Xavier, 524 (sexto andar), Maracanã, Rio de Janeiro, RJ 20559-900 (Brazil), Tel. +55 212 334 0144, E-Mail ccortez@uerj.br
                Article
                328331 Kidney Blood Press Res 2011;34:424–429
                10.1159/000328331
                21709423
                131e2cae-f0d1-480a-a50f-cf0dde930406
                © 2011 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 13 July 2010
                : 01 April 2011
                Page count
                Figures: 3, Tables: 2, Pages: 6
                Categories
                Original Paper

                Cardiovascular Medicine,Nephrology
                Kidney injury,Renal morphology,Nephron number,Creatinine,Stress
                Cardiovascular Medicine, Nephrology
                Kidney injury, Renal morphology, Nephron number, Creatinine, Stress

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