Literature DB >> 2578725

Basic cellular mechanisms of action of the calcium-channel blockers.

A M Katz.   

Abstract

Calcium-channel blockers inhibit the entry of calcium ion (Ca++) into excitable cells, including those of coronary and peripheral arterial smooth muscle and the heart. The ability of these drugs to block Ca++ entry into cells inhibits the essential role of this cation as an intracellular messenger. The effects of calcium-channel blockers on the heart include a negative inotropic effect on the working myocardial cells of the atria and ventricles. Because the up-stroke of the action potential in these regions of the heart, and in the rapidly conducting cells of the His-Purkinje system, is due to a fast, sodium-dependent ionic current, calcium-channel blockers do not inhibit conduction in these cells. In the sinoatrial and atrioventricular (AV) nodes, on the other hand, depolarization is due primarily to a Ca++-dependent slow inward current; as a result, the calcium-channel blockers inhibit the sinus pacemaker and AV conduction. Because our knowledge of the molecular structure of the calcium channels in the heart and smooth muscle is rudimentary, little is known of the molecular mechanisms by which calcium-channel blockers inhibit Ca++ entry across the sarcolemmal membranes in these cells. It is apparent, however, that the actions of different members of this class of drugs on the sarcolemma are not the same. Indirect evidence indicates that some members of this class of drugs may interact with hydrophobic regions of the proteins that make up, or regulate, the calcium channels in the plasma membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1985        PMID: 2578725     DOI: 10.1016/0002-9149(85)90607-1

Source DB:  PubMed          Journal:  Am J Cardiol        ISSN: 0002-9149            Impact factor:   2.778


  6 in total

1.  The Novel Development of an Experimental Model of Dihydropyridine Calcium Channel Blocker Poisoning using Intravenous Amlodipine.

Authors:  David Jang; Sean Donovan; Theodore Bania; Lewis Nelson; Robert Hoffman; Jason Chu
Journal:  Int J Cardiovasc Res       Date:  2013-03-29

2.  Regulation of Ca2+ homeostasis by glucose metabolism in rat brain.

Authors:  M Nijjar; R L Belgrave
Journal:  Mol Cell Biochem       Date:  1997-11       Impact factor: 3.396

3.  Protection by verapamil and nifedipine against ischaemia-induced loss of [3H]-(+)-PN 200-110 binding sites in the rat heart.

Authors:  F T van Amsterdam; M S van Amsterdam-Magnoni; M Haas; N C Punt; J Zaagsma
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  1990 Jan-Feb       Impact factor: 3.000

4.  Lack of effect of nicardipine and diltiazem on glucose- and arginine-induced insulin release in obese subjects.

Authors:  A Pezzarossa; M C Cimicchi; N Orlandi; A Gnudi; C Manca; A Perrone; R Bolognesi
Journal:  Cardiovasc Drugs Ther       Date:  1988-12       Impact factor: 3.727

5.  Beneficial effects of verapamil during metabolic acidosis in isolated perfused rat hearts.

Authors:  W Markiewicz; S S Wu; R Sievers; W W Parmley; T A Watters; T L James; C B Higgins; J Wikman-Coffelt
Journal:  Cardiovasc Drugs Ther       Date:  1988-01       Impact factor: 3.727

6.  Effect of Ca2+ channel blockers, external Ca2+ and phospholipase A2 inhibitors on t-butylhydroperoxide-induced lipid peroxidation and toxicity in rat liver slices.

Authors:  J Heo; G H Kim; K S Lee; W U Go; H J Ju; S K Park; C S Song; G A Song; M Cho; U S Yang; H K Moon; Y K Kim
Journal:  Korean J Intern Med       Date:  1997-06       Impact factor: 2.884

  6 in total

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