Revising the question of receptor specificity of opioidergic increases of heart electrical stability in the adaptation of rats to stress and hypobaric hypoxia

It has been found that the adaptation to the intermitted immobilization stress or chronic hypobaric hypoxia leads to the increase of cardiac tolerance to the arrhythmogenic action of coronary artery occlusion and reperfusion. The antiarrhythmic effect of adaptation to stress was neutralized using the ƒ-antagonist, CTAP (0.5 mg/kg, i.v.) injection. Selective ƒ- or ƒ-antagonists had no effect on stress adaptive cardiac resistance to arrhythmogenic action of ischemia and reperfusion. Inhibition of d-opioid receptors by intravenous administration of the selective ƒ opioid antagonist TIPP(ƒ) (0.5 mg/kg, i.v.) completely abolished the antiarrhythmic effect of adaptation to hypoxia. Inhibition of ƒ-opioid receptors by CTAP (0.5 mg/kg, i.v.) or ƒ-receptors by norbinaltorphimine (9 mg/kg, i.v.) had no effect on the incidence of heart rhythm disturbances in hypoxic adapted rats during coronary artery occlusion and reperfusion. It was concluded that the antiarrhythmic effect of adaptation to chronic stress is mediated via ƒ-opioid receptors, the antiarrhythmic effect of adaptation to chronic hypobaric hypoxia is mediated via ƒ-opioid receptors.