Blog
About

0
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Mechanism of Vasopressin-Induced Contraction of Renal Medullary Interstitial Cells

      a , b

      Nephron Physiology

      S. Karger AG

      Medulla, Urine concentration, Prostaglandin E2

      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: Previous studies have identified a contractile function for renomedullary interstitial cells (RMIC). Such studies focused on the mechanism of endothelin-1-induced RMIC contraction; however, vasopressin (AVP) was also noted to contract RMIC. Since AVP-induced RMIC contraction may be relevant to the medullary effects of AVP on urinary concentration, these initial observations have been extended to examination of the mechanism of AVP-induced RMIC contraction. Methods: Cultured rat RMIC were exposed to AVP and other agents, and examined using video microscopy. Results: AVP caused a slowly developing and dose-dependent reduction in RMIC surface area. AVP-induced RMIC contraction was abolished by blockade of V<sub>1</sub>, but not V<sub>2</sub>, receptors. Nifedipine and nickel reduced AVP-stimulated RMIC contraction, indicating that this effect is dependent upon dihydropyridine-sensitive calcium channels. H7, a protein kinase C inhibitor, completely abrogated AVP action, while the nitric oxide synthase inhibitor, NMMA, had no effect. Indomethacin enhanced AVP-induced RMIC contraction, and addition of PGE<sub>2</sub> together with indomethacin reduced AVP action. Conclusion: These data indicate that AVP potently contracts RMIC via V<sub>1</sub> receptor stimulation of PKC and intracellular calcium accumulation, and that AVP-stimulated prostaglandin production downregulates the contractile effect of AVP on RMIC. AVP modulation of RMIC contraction may be involved in the regulation of urinary concentration.

          Related collections

          Most cited references 17

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

          Anatomy of the renal interstitium.

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

            Therapeutic potential of protein kinase C inhibitors.

            The serine/threonine protein kinase, protein kinase C (PKC) is a family of closely related isoforms which are physiologically activated by diacylglycerol generated by the binding of a variety of agonists to their cellular receptors. Free fatty acids may also play a role in activating PKC. The enzyme apparently mediates a wide range of signal transduction processes in cells and, therefore, inhibitors directed selectively against PKC may have wide-ranging therapeutic potential. This review highlights the evidence that inappropriate activation of PKC occurs in a number of disease states. Such evidence, however, is often seriously flawed because it relies on the use of phorbol esters, which are potent and direct PKC activators but may not mimic the physiological triggering of the enzyme in cells, or on the use of non-selective protein kinase inhibitors such as H7 and staurosporine. A new generation of bis-indolylmaleimides, derived from the lead provided by staurosporine, shows a high degree of selectivity for PKC over closely related protein kinases and such agents may provide more appropriate tools to investigate the role of PKC in cellular processes.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              Inhibitors of Na-K-ATPase in human urine: effects of ouabain-like factors and of vanadium-diascorbate on calcium mobilization in rat vascular smooth muscle cells*1

                Bookmark

                Author and article information

                Journal
                NEP
                Nephron Physiol
                10.1159/issn.1660-2137
                Nephron Physiology
                S. Karger AG
                1660-2137
                2006
                June 2006
                22 June 2006
                : 103
                : 3
                : p119-p124
                Affiliations
                aDepartment of Veterans Affairs Medical Center, bDivision of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah, USA
                Article
                92245 Nephron Physiol 2006;103:p119–p124
                10.1159/000092245
                16557030
                © 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.

                Page count
                Figures: 5, References: 24, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/92245
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Medulla, Urine concentration, Prostaglandin E2

                Comments

                Comment on this article