Dopamine Receptor Mediated Hypothermic Action of B-HT 920 in Rats

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Abstract
— The hypothermic action of the thiazoloazepine derivative B‐HT 920, an α2‐adrenoceptor agonist has been investigated in rats. B‐HT 920 (6‐allyl‐2‐amino‐5,6,7,8‐tetrahydro‐4H‐thiazolo‐(4,5‐d)‐azepine dihydrochloride) (0·25–10 mg kg−1 i.p.) induced a dose‐dependent hypothermia. The peak effect was seen within 60·90 min and lasted up to 120 min. Its action was potentiated by the selective D1‐dopamine agonist SKF 38393 and inhibited by the D2‐anatagonists haloperidol (1 mg kg−1) and sulpiride (100 mg kg−1). The hypothermic action of B‐HT 920 was centrally mediated; i.c.v. administration of 10 μg produced a significant fall in rectal temperature which was sensitive to blockade by haloperidol. B‐HT 920 also potentiated the hypothermic action of apomorphine (0·1 and 0·5 mg kg−1) in a haloperidol sensitive manner. Reserpine (5 mg kg−1 i.p.) pretreatment reduced the hypothermic response of B‐HT 920 (0·5 mg kg−1) but sensitized the response due to the combination of B‐HT 920 (0·5 mg kg−1) and apomorphine (0·1 mg kg−1). Neither the selective α2‐adrenoceptor antagonists, yohimbine (1 mg kg−1) or idazoxan (1 mg kg−1), the histamine antagonist mepyramine (10 mg kg−1) nor the 5‐HT antagonist cyproheptadine (5 mg kg−1) inhibited B‐HT 920‐induced hypothermia. Similarly, the selective α1‐antagonist prazosin (1 mg kg−1) and the β‐antagonist propranolol (10 mg kg−1) failed to modify the hypothermic action of B‐HT 920. These observations demonstrated hypothermia induced by B‐HT 920 is mediated by postsynaptic D2‐receptors and D1‐ and D2‐receptor interplay is essential for the full expression of hypothermia in rats.

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