Blog
About

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

      Regulation of Renal A 1 Adenosine Receptors in vivo

      Read this article at

      ScienceOpenPublisher
      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

          We have compared renal A<sub>1</sub> adenosine receptor (AR) regulations in rats after chronic agonist and antagonist treatments. In one group, R-phenylisopropyladenosine (R-PIA), a selective A<sub>1</sub> AR agonist, was infused subcutaneously for 7 days. Another group was fed theophylline, a non-selective AR antagonist, for 2 weeks. Renal cortex membrane A<sub>1</sub> AR binding with 1,3-[<sup>3</sup>H]-dipropyl-8-cyclopentylxanthine demonstrated ∼40% reduction in the B<sub>max </sub> for the R-PIA group without any changes in the K<sub>d</sub> values. Neither the B<sub>max</sub> nor the K<sub>d</sub> changed following chronic theophylline treatment. Renal cortex G<sub>i</sub>α-proteins from the R-PIA treated rats decreased by ∼30%. Renal G<sub>i</sub>α levels did not change in theophylline-treated rats. Consistent with the A<sub>1</sub> AR desensitization, R-PIA-treated rats had significantly higher basal renin release and showed attenuated A<sub>1</sub> AR-mediated inhibition of renin release. These data suggest that prolonged A<sub>1</sub> AR stimulation results in downregulation of renal A<sub>1</sub> ARs and G<sub>i</sub>α, accompanied by desensitization of A<sub>1</sub> AR-mediated inhibitory effects on renin release. Unlike cardiac and brain A<sub>1</sub> ARs, renal A<sub>1</sub> receptors are not subject to up-regulation following chronic antagonist treatment.

          Related collections

          Most cited references 2

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

          Central effects of caffeine on renal renin secretion and norepinephrine spillover.

          Endogenous adenosine in the brain may inhibit central sympathetic tone and thereby restrain renin release, a mechanism that may be particularly important when sympathetic activity is enhanced. The purpose of our study was to test the hypothesis that the adenosine receptor antagonist caffeine increases renin release in part by disabling the central nervous system (CNS) adenosine brake on renin release. This hypothesis was tested by conducting three protocols in anesthetized rats. In the first protocol, intracerebroventricular (i.c.v.) infusions of caffeine (10 micrograms/kg/min) did not alter either bradycardic responses to intravenous (i.v.) infusion of N6-cyclopentyladenosine (CPA, A1-receptor agonist) or depressor responses to i.v. infusions of CGS21680 (A1-receptor agonist). However, i.c.v. caffeine did block bradycardic responses to i.c.v. boluses of CPA and depressor responses to i.c.v. boluses of CGS21680, thus demonstrating that i.c.v. caffeine at the dose used blocks CNS but not peripheral adenosine receptors. In the second protocol, hydralazine (1 and 10 mg/kg, administered intraperitoneally) significantly enhanced both the renal secretion of renin and the renal spillover of norepinephrine (NE), thus confirming that hydralazine can increase renin release by unloading arterial baroreceptors and increasing sympathetic tone to the kidneys. In the third protocol, the effects of i.c.v. caffeine (10 micrograms/kg/min) on hydralazine-induced (1 and 10 mg/kg, administered intraperitoneally) changes in renal secretion of renin and renal NE spillover were investigated. In this protocol, i.c.v. caffeine did not alter baseline values for either the renal secretion of renin or NE. In contrast, i.c.v. caffeine significantly (p = 0.03) enhanced the increase in renal renin secretion induced by 1 and 10 mg/kg hydralazine (for 1 mg/kg hydralazine delta of 6.4 +/- 46.7 and 142.4 +/- 142.9 renin activity/min/kg body weight in control and caffeine-treated animals, respectively; for 10 mg/kg hydralazine, delta 227.8 +/- 73.9 and 600.8 +/- 168.9 renin activity/min/kg body weight in control and caffeine-treated animals, respectively). The enhanced renin-secretion response to hydralazine in caffeine-treated rats was accompanied by augmented hydralazine-induced increase in renal NE spillover (p = 0.035). These data strongly support the hypothesis of a CNS adenosine brake on renin release that is disabled by caffeine.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Chronic exposure to subcutaneously implanted methylxanthines

              Bookmark

              Author and article information

              Journal
              EXN
              Nephron Exp Nephrol
              10.1159/issn.1660-2129
              Cardiorenal Medicine
              S. Karger AG
              1660-2129
              2002
              2002
              09 January 2002
              : 10
              : 1
              : 43-50
              Affiliations
              aDepartment of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, N.Y., and bDepartment of Physiology, New York Medical College, Valhalla, N.Y., USA
              Article
              49897 Exp Nephrol 2002;10:43–50
              10.1159/000049897
              © 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, References: 34, Pages: 8
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/49897
              Categories
              Original Paper

              Comments

              Comment on this article