Bradykinin plays a role in the regulation of coronary blood flow. Under basic conditions the vasodilating effect is primarily mediated by stimulation of the endogenous nitrovasodilator endothelium-derived relaxing factor (EDRF). This effect is shortlasting but can be increased and prolonged by sulfhydryl(SH)-containing agents. ACE-inhibitors may cause coronary vasorelaxation by a bradykinin-mediated release of EDRF. This can be potentiated by the presence of SH-groups, as was shown with captopril and zofenoprilat. As a consequence, SH-containing ACE-inhibitors may potentiate nitrates, because they act as exogenous nitrovasodilators, and reverse tolerance to their therapeutic effect.