4
views
0
recommends
+1 Recommend
1 collections
    0
    shares

      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found

      Flow-Associated Dilatory Capacity of the Brachial Artery Is Intact in Early Autosomal Dominant Polycystic Kidney Disease

      research-article

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background/Aims: Autosomal dominant polycystic kidney disease is associated with endothelial dysfunction of resistance arteries. This study tested whether endothelial dysfunction is also present in the conduit arteries in patients with preserved renal function. Methods:Twenty-seven patients (9 females and 18 males, age 36 ± 10 years) with polycystic kidney disease and normal renal function were compared to 27 healthy controls. The dilatory responses of the brachial artery to postischemic increased blood flow [endothelium-dependent flow-associated dilatation (FAD)] and to nitroglycerin [endothelium-independent nitroglycerin-induced dilatation (NID)] were measured by external ultrasound. Plasma concentrations of the stable end products of nitric oxide nitrate/nitrite (NOx) and of the endothelial markers vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1, E-selectin and von Willebrand factor antigen were also measured. Results:No differences in FAD or NID were found between patients and controls (104.6 ± 4.2 vs. 105.3 ± 3.9%, mean ± SD, p = 0.55, and 117.0 ± 8.4 vs. 117.5 ± 7.6%, p = 0.75). However, the plasma concentration of VCAM-1 was elevated and the plasma concentration of NOx was reduced in patients with polycystic kidney disease. Conclusion: Biochemical markers confirm an association between polycystic kidney disease and endothelial dysfunction. However, a normal FAD of the brachial artery suggests that the endothelial dysfunction does not involve the conduit arteries.

          Related collections

          Most cited references15

          • Record: found
          • Abstract: not found
          • Article: not found

          Non-invasive measurement of human endothelium dependent arterial responses: accuracy and reproducibility.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Endothelium-dependent contractions in hypertension.

            1. Endothelial cells, under given circumstances, can initiate contraction (constriction) of the vascular smooth muscle cells that surround them. Such endothelium-dependent, acute increases in contractile tone can be due to the withdrawal of the production of nitric oxide, to the production of vasoconstrictor peptides (angiotensin II, endothelin-1), to the formation of oxygen-derived free radicals (superoxide anions) and/or the release of vasoconstrictor metabolites of arachidonic acid. The latter have been termed endothelium-derived contracting factor (EDCF) as they can contribute to moment-to-moment changes in contractile activity of the underlying vascular smooth muscle cells. 2. To judge from animal experiments, EDCF-mediated responses are exacerbated by aging, spontaneous hypertension and diabetes. 3. To judge from human studies, they contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. 4. Since EDCF causes vasoconstriction by activation of the TP-receptors on the vascular smooth muscle cells, selective antagonists at these receptors prevent endothelium-dependent contractions, and curtail the endothelial dysfunction in hypertension and diabetes.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Endothelial dysfunction and reduced nitric oxide in resistance arteries in autosomal-dominant polycystic kidney disease.

              Patients with autosomal-dominant polycystic kidney disease (ADPKD) have defective endothelium-dependent relaxation (EDR). We investigated the relationship between endothelial dysfunction and nitric oxide generation in hypertension and chronic renal insufficiency (CRI) in ADPKD. We contrasted acetylcholine (ACh)-induced EDR, 3-morphollinosydnonimine (SIN-1)-induced endothelium-independent relaxation (EIDR) and constitutive nitric oxide synthase (cNOS) activity in subcutaneous resistance vessels and plasma levels and excretion of NO2-/NO3- (NOX) in normal, control (N = 10) patients with ADPKD or essential hypertension. EDR was decreased significantly in normotensive ADPKD (N = 9), but more severely in hypertensive ADPKD (N = 6), or those with CRI (N = 5) and in essential hypertension (N = 9). The increases in EDR with l-arginine and decreases with LG-nitro-l-arginine methyl ester (L-NAME) were lost in all groups of patients with ADPKD and in essential hypertension except for a modest effect of L-NAME in normotensive ADPKD. EIDR was unimpaired throughout. Vascular cNOS activity and renal NOX excretion were reduced profoundly in patients with all categories of ADPKD and especially in those with hypertension. EDR in resistance vessels from patients with ADPKD is impaired even in the absence of hypertension or CRI, but becomes more marked as hypertension develops. Patients with ADPKD have defective nitric oxide generation from diminished cNOS activity. Endothelial dysfunction and impaired cNOS activity in ADPKD may predispose to hypertension whose occurrence is accompanied by a further sharp deterioration in EDR.
                Bookmark

                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2006
                September 2006
                15 September 2006
                : 26
                : 4
                : 335-339
                Affiliations
                Departments of Nephrology, aRigshospitalet, University of Copenhagen, Copenhagen, and bHerlev University Hospital, Herlev, Denmark
                Article
                94402 Am J Nephrol 2006;26:335–339
                10.1159/000094402
                16825759
                280511ab-1611-4695-a2ad-a3fe6d7121bc
                © 2006 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
                : 30 March 2006
                : 05 June 2006
                Page count
                Tables: 3, References: 23, Pages: 5
                Categories
                Original Report: Patient-Oriented, Translational Research

                Cardiovascular Medicine,Nephrology
                Blood flow,Endothelial dysfunction,Autosomal dominant polycystic kidney disease,Renal function,Dilatory responses

                Comments

                Comment on this article