ORIGINAL ARTICLE: PDF OnlyZucchi Riccardo; Ronca-Testoni, Simonetta; Ugo, Limbruno; Yu, Gongyuan; Galbani, Paola; Ronca, Giovanni and; Mario, MarianiJournal of Cardiovascular Pharmacology: 1992 - p 11-15 Free Abstract Summary We investigated the effect of gallopamil on cardiac sarcoplasmic reticulum (SR) function. Heavy SR was prepared from bovine ventricular muscle. Oxalate-supported calcium uptake was stimulated by gallopamil at concentrations ranging from 10 to 300 nM, whereas higher concentrations were ineffective. Peak stimulation averaged 25–30% of control calcium uptake and was observed at free calcium concentrations ranging from I to 6 μM Calcium uptake is actually the difference between active calcium transport by SR calcium-adenosine triphosphatase (calcium-ATPase), and passive efflux through SR calcium-release channels. In the presence of 300 μM of ryanodine, a blocker of SR channels, calcium uptake increased by 43% under control conditions, but no further stimulation was produced by gallopamil. SR calcium-ATPase was not affected by gallopamil. Similar results were obtained when oxalate-supported calcium uptake was determined with use of unfractionated homogenate obtained from rat hearts. We conclude that gallopamil acts on SR calcium-release channels and reduces the probability of channel opening and/or channel conductivity. The dose-response curve is bell shaped, and the maximum effect, which corresponds to 65% of the maximum effect of ryanodine, is achieved at therapeutic concentrations. Such action might contribute to the beneficial effect of gallopamil in the treatment of myocardial ischemia. Copyright © 1992 Wolters Kluwer Health, Inc. All rights reserved.