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      Effect of a High Salt Diet on Microvascular Antioxidant Enzymes

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      Journal of Vascular Research

      S. Karger AG

      Nitric oxide, Free radicals, Microcirculation, Endothelium, Dietary salt

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          Abstract

          High dietary salt intake decreases the endothelium-dependent dilation of skeletal muscle arterioles by inhibiting local nitric oxide (NO) activity without changing vascular smooth muscle responsiveness to NO. Under these conditions, microvascular walls show evidence of oxidative stress, and scavengers of reactive oxygen species (ROS) abolish this oxidative stress and restore normal arteriolar responses to acetylcholine (ACh). We tested the hypothesis that the salt-dependent appearance of microvascular ROS, and accompanying reduction in endothelium-dependent dilation, is due to a decrease in antioxidant enzyme expression or activity. We studied spinotrapezius muscle microvessels in rats fed normal (NS) (0.45%) or high (HS) (7%) salt diets for 4–5 weeks. Western analysis of arteriolar and venular protein showed no difference between groups in the content of superoxide dismutase (Cu/Zn SOD), catalase, or glutathione peroxidase. The catalase inhibitor 3-amino-1,2,4-triazole (3AT) increased arteriolar and venular oxidant activity (assessed by tetranitroblue tetrazolium reduction) by the same amount in both groups, suggesting similar levels of catalase activity. 3AT did not affect arteriolar responses to ACh in either group. The Cu/Zn SOD inhibitor diethyldithiocarbamate increased arteriolar and venular oxidant activity to a lesser extent in HS rats, suggesting reduced Cu/Zn SOD activity in this group. Cu/Zn SOD inhibition decreased arteriolar responses to ACh only in NS rats. These findings suggest that endogenous Cu/Zn SOD preserves the endothelium-dependent control of arteriolar tone in NS rats, and that a reduction in Cu/Zn SOD activity contributes to the loss of arteriolar NO activity in HS rats.

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          Most cited references 3

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          Effect of salt loading on nitric oxide synthase expression in normotensive rats.

           N. Vaziri,  Z. J. Ni (2001)
          Elevation of arterial blood pressure (BP) with high salt intake in Dahl salt-sensitive rats is associated and perhaps, in part, due to downregulation of renal and vascular production of nitric oxide (NO) and nitric oxide synthase (NOS) expressions. Several recent studies have revealed a significant increase in BP in Sprague-Dawley rats on high salt intake. Given the apparent salt sensitivity of Sprague-Dawley rats, we hypothesized that chronic high salt intake may affect NO system in these rats in a manner resembling that reported in salt-sensitive (not salt-resistant) Dahl rats. The effects of a high salt diet (chow containing 8% NaCl) of 48-h or 3-week duration was studied on immunodetectable endothelial (eNOS), inducible (iNOS), and neuronal (nNOS) NOS expressions of relevant organs in male Sprague-Dawley rats. The results were compared with those obtained in the control animals fed a regular no-added salt diet (0.2% NaCl). Consumption of a high salt diet for 3 weeks induced hypertension (HTN) (158 +/- 6 v 115 +/- 5 mm Hg, P < .01) and widespread downregulation of iNOS expression in renal cortex, renal medulla, aorta, and heart. Similarly, chronic salt loading resulted in marked downregulation of eNOS expression in renal cortex and aorta and lowered expressions of nNOS in the brain, renal cortex, and renal medulla. In comparison, short-term salt loading resulted in significant reduction of iNOS in the renal cortex and aorta and of eNOS in the aorta together with significant elevation of nNOS expression in renal medulla and brain. Thus, chronic consumption of a high salt diet resulted in moderate HTN in normotensive Sprague-Dawley rats. This was accompanied by widespread downregulation of various NOS isotypes that undoubtedly contributed to the development and maintenance of HTN in this model.
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            Effect of oxygen tension on regulation of arteriolar diameter in skeletal muscle in situ.

             K Klotz,  K Ley,  P Gaehtgens (1995)
            Skeletal muscle arterioles are known to constrict upon elevation of ambient PO2. While several studies have shown that the endothelium plays an important role in this response, it is not clear how this response is mediated. We examined the oxygen-induced constriction of arterioles in the rat spinotrapezius muscle. Elevation of superfusion solution PO2 from about 15 to 150 mm Hg caused arteriolar constriction by 25% (+/- 3%, n = 18). Inhibition of prostaglandin synthesis by superfusion of indomethacin (30 microM) produced vasoconstriction by 28% (+/- 9.5%, n = 5), but left the PO2 response unaffected. Blockade of the synthesis of endothelium-derived relaxing factor (EDRF) by NG-nitro-L-arginine (L-NNA, 35 mg/kg i.v.) caused arteriolar constriction by 31% (+/- 8%, n = 8). During application of L-NNA, the constrictor response to PO2 elevation was reduced to 3 +/- 2%. Administration of superoxide dismutase (SOD, 80,000 U/kg i.v.) did not affect the PO2 response. It is concluded that in small arterioles of skeletal muscle both EDRF and prostanoids sustain a significant basal dilatation. The dilatory effects of EDRF but not of prostaglandins are strongly dependent on PO2. The vasoconstriction in response to high ambient PO2 is not due to EDRF breakdown during its diffusion from endothelial to smooth muscle cells.
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              • Record: found
              • Abstract: not found
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              Chronic Elevations in Salt Intake and Reduced Renal Mass Hypertension Compromise Mechanisms of Arteriolar Dilation

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                Author and article information

                Journal
                JVR
                J Vasc Res
                10.1159/issn.1018-1172
                Journal of Vascular Research
                S. Karger AG
                1018-1172
                1423-0135
                2002
                February 2002
                13 February 2002
                : 39
                : 1
                : 41-50
                Affiliations
                Department of Physiology, West Virginia University School of Medicine, Morgantown, W.Va., USA
                Article
                48992 J Vasc Res 2002;39:41–50
                10.1159/000048992
                11844936
                © 2002 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.

                Page count
                Figures: 6, Tables: 1, References: 54, Pages: 10
                Categories
                Research Paper

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