Intracisternal administration of pergolide, a dopamine receptor agonist, triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-dependent adenosine triphosphatase and enhances vascular reactivity in anaesthetized dogs.

1. The present studies were undertaken to investigate whether intracisternal administration of pergolide, a dopamine-2 receptor agonist, triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-dependent adenosine triphosphatase into the circulation and whether such an effect is associated with increases in vascular reactivity in pentobarbital anaesthetized dogs. In different groups of animals, Na+-pump activity was estimated in the plantar and dorsal branches of the lateral saphenous veins by using the 86Rb-uptake method; vascular responsiveness to noradrenaline was studied in the denervated perfused hindlimb. 2. Na+-pump activity was significantly depressed in those blood vessels which were collected at 90 min after central administration of pergolide (12.5 micrograms/kg intracisternally). In perfused hindlimb studies, vascular responses to noradrenaline were significantly enhanced between 60 and 90 min after pergolide. Since the Na+-pump activity was evaluated in the hindlimb veins, and vascular reactivity was studied on the arterial circulation, the data suggest that the changes in both these variables could have been caused by a circulating substance. 3. In separate series of experiments, plasma samples were collected before and after intracisternal administration of pergolide. The Na+-pump activity was significantly inhibited in the segments of lateral saphenous veins which were incubated in the fresh plasma and/or boiled plasma supernatants, indicating that a heat stable pump inhibitor(s) is released into the circulation after pergolide administration. 4. Effects of pergolide demonstrated in the present study are qualitatively similar to those reported to occur after acute blood volume expansion. Hence it is proposed that central dopaminergic mechanisms may play an intermediary role in the release of the Na+-pump inhibitor(s).(ABSTRACT TRUNCATED AT 250 WORDS)