DENSITY OF L-TYPE CALCIUM CHANNELS IN ISCHEMICALLY PRECONDITIONED PORCINE HEART REGIONS

Ischaemic preconditioning by brief ischaemic episodes could be explain ed by reduced cellular calcium ion (Ca2+) influx, reduced cytosolic Ca 2+ overload and delayed cell-injury during subsequent long-lasting isc haemia. L-type calcium channels (LCC) regulate sarcolemmal Ca2+ influx in myocardial cells. The aim of this study was to investigate if prec onditioning was associated with reduced density or altered state of LC C in the preconditioned region of the heart. To test this Ne compared the density and the dissociation constant of(+)-[H-3]isradipine bindin g to LCC in membranes from preconditioned and control regions of porci ne 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 ci rcumflex artery at the end of the last reperfusion, and (+)-[H-3]israd ipine binding to membranes made from the biopsies was measured. The di fferences in density and dissociation constant of (+)-[H-3]isradipine binding to LCC in membranes from preconditioned and control regions we re not significant. In conclusion, the proposed effect of ischaemic pr econditioning to reduce Ca2+ influx, does not involve local changes in density or state of LCC that could be detected by (+)-[H-3]isradipine binding.