+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      An Overview of Slow Channel Blocking Drugs: Pharmacological Basis for Therapeutic Applications


      S. Karger AG

      Calcium antagonists, Coronary dynamics, Vasospasm, Stable and unstable angina, Arrhythmias

      Read this article at

          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.


          The use of voltage clamps in cardiac muscle has permitted the separation of two inward depolarizing membrane currents. The first is the fast sodium current, with rapid kinetics of activation and inactivation, which is blocked by local anesthetics. The second is the slow current carried largely by calcium ions, having slow kinetics with a long time constant of inactivation. Agents which selectively block this current are called Ca antagonists. Such agents are heterogeneous structurally; they also block calcium currents in smooth muscle and therefore produce coronary as well as peripheral vasodilatation. The most significant agents are verapamil, gallopamil, nifedipine, diltiazem and tiapamil. They have a varying spectrum of pharmacological effects with respect to changes they produce on heart rate, afterload, preload, contractility, coronary flow and on the AV node. A similar spectrum of therapeutic effects is apparent in different clinical disorders, in particular vasospastic angina, stable and unstable angina, cardiac arrhythmias, hypertension, hypertrophic cardiomyopathy and possibly other disorders. Indeed, the full range of clinical disorders which may respond to calcium antagonists is still not fully delineated and may well be at least as extensive as that for β-adrenoceptor blocking drugs. The advent of calcium antagonists in the last decade represents one of the most significant advances in cardiovascular therapeutics.

          Related collections

          Author and article information

          S. Karger AG
          07 November 2008
          : 69
          : Suppl 1
          : 2-25
          UCLA School of Medicine and Cardiovascular Research Laboratory, Wadsworth VA Medical Center, Los Angeles, Calif., USA
          173534 Cardiology 1982;69:2–25
          © 1982 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
          Pages: 24


          Comment on this article