The results obtained in a variety of isolated organ preparations characterize tiapamil as a calcium antagonist or calcium entry blocker. Tiapamil inhibited in a concentration-dependent manner calcium-induced contractions in isolated, potassium-depolarized preparations of rat renal artery, dog coronary artery and rabbit main pulmonary artery and reduced 45Ca influx into depolarized vascular smooth muscle cells. The inhibitory effects of tiapamil were surmountable by an elevation of the extracellular calcium concentration. Calcium-mediated, slowly rising potentials in partially depolarized guinea pig papillary muscle, evoked by electrical stimulation in the presence of isoprenaline, were also antagonized by tiapamil. As in vascular muscle, the tiapamil effects in cardiac muscle were reduced by elevation of external calcium.Tiapamil altered haemodynamic parameters in a characteristic sequence, with an increase in coronary flow appearing at the lowest effective doses, followed by decreases in blood pressure, total peripheral vascular resistance and, eventually, heart rate. A depression of myocardial contractility was not found at doses which are considered to be therapeutic. After cardiac autonomic denervation, tiapamil produced a dose-dependent bradycardia. However, cardiac denervation did not alter the extent of tiapamil-induced decreases in coronary vascular resistance and did not unmask a potential negative inotropic effect of the drug. A comparison of various vascular preparations suggested a certain degree of selectivity for coronary arteries in the calcium antagonistic action of tiapamil. The haemodynamic findings are in line with these in vitro results.A coronary segmental analysis revealed that tiapamil acts on small coronary arteries. It differs in this respect from nitroglycerin which dilates large coronary arteries. Tiapamil increased pO2 in the subendocardial layers of the myocardium percentagewise more than in the subepicardial layers. Furthermore, it reduced experimentally-induced myocardial ischaemia as determined by a reduction of the S-T segment elevation of the epicardial ECG after ligation of a coronary artery.

This content is only available via PDF.
Copyright / Drug Dosage / Disclaimer
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.
You do not currently have access to this content.