Density of L-type calcium channels in ischaemically preconditioned porcine heart regions

Ischaemic preconditioning by brief ischaemic episodes could be explained by reduced cellular calcium ion (Ca2+) influx, reduced cytosolic Ca2+ overload and delayed cell-injury during subsequent long-lasting ischaemia. L-type calcium channels (LCC) regulate sarcolemmal Ca2+ influx in myocardial cells. The aim of this study was to investigate if preconditioning was associated with reduced density or altered state of LCC in the preconditioned region of the heart. To test this we compared the density and the dissociation constant of (+)-[3H]isradipine binding to LCC in membranes from preconditioned and control regions of porcine hearts. Eight porcine hearts were regionally preconditioned by two 10-min occlusions of the mid left anterior descending artery, and each occlusion was followed by 30 min of reperfusion. Biopsies were taken from the preconditioned regions and control regions supplied by the circumflex artery at the end of the last reperfusion, and (+)-[3H]isradipine binding to membranes made from the biopsies was measured. The differences in density and dissociation constant of (+)-[3H]isradipine binding to LCC in membranes from preconditioned and control regions were not significant. In conclusion, the proposed effect of ischaemic preconditioning to reduce Ca2+ influx, does not involve local changes in density or state of LCC that could be detected by (+)-[3H]isradipine binding.