ABSTRACT
Intracerebroventricularly administered dopamine produced dose dependent hyperthermia in rabbits. Haloperidol, a D1 receptor blocker produced consistent hypothermia, whereas D2 receptor blocker metoclopramide produced hyperthermia, pretreatment with haloperidol competitively blocked the hyperthermic response of dopamine. Pretreatment with metoclopramide augmented the onset and peak response of dopamine. It is suggested that D1 receptors are involved in producing hyperthermia and D2 receptors in hypothermia.
Subject(s)
Animals , Body Temperature Regulation/drug effects , Female , Haloperidol/pharmacology , Male , Metoclopramide/pharmacology , Rabbits , Receptors, Dopamine/physiologyABSTRACT
Haloperidol administration (iv) has been shown to produce miosis in dogs. In the present study on rabbits, haloperidol administration (iv) produced dose-related miosis but when administered intracerebroventricularly, it failed to produce any change in pupillary size. Higher degree of miosis was observed when haloperidol was administered directly into the anterior chamber of eye. Haloperidol pretreatment failed to significantly modify the mydriasis produced by phenylephrine or atropine. These observations suggest that the miosis produced by haloperidol is a peripheral effect, and also that the miosis is not mediated through the blockade of alpha adrenoceptors of radial muscles or stimulation of cholinoceptors of circular muscles of iris.
Subject(s)
Animals , Atropine/pharmacology , Female , Haloperidol/administration & dosage , Injections, Intravenous , Injections, Intraventricular , Male , Miosis/chemically induced , Mydriasis/chemically induced , Phenylephrine/pharmacology , RabbitsABSTRACT
Intracerebroventricular (icv) injection of methyldopa induced body temperature changes in the rabbits. The dose of 100 micrograms/kg did not produce any significant change on body temperature whereas 250 micrograms/kg of the drug induced hyperthermia. Higher dose of 500 micrograms/kg produced initial hypothermia which was followed by hyperthermia. On further increase of the dose to 1 mg/kg, consistent hypothermia was evident. Prazosin, a specific post-synaptic alpha 1 adrenoceptor blocker, induced hypothermia whereas piperoxan (presynaptic alpha 2 antagonist) produced hyperthermia. The pretreatment with prazosin, blocked the hyperthermic response of methyldopa. The initial hypothermia by 500 micrograms/kg of methyldopa was also potentiated. The pretreatment with piperoxan completely blocked the hypothermia but had no effect on hyperthermic response of methyldopa. Pretreatment of rabbits with both prazosin and piperoxan completely blocked the hypothermia as well as hyperthermic response of methyldopa. Thus it appeared that both presynaptic alpha 2 and postsynaptic alpha 1 adrenoceptors are involved in central thermoregulation in rabbits.
Subject(s)
Adrenergic alpha-Antagonists/pharmacology , Animals , Body Temperature/drug effects , Body Temperature Regulation/drug effects , Female , Male , Methyldopa/pharmacology , Piperoxan/pharmacology , Prazosin/pharmacology , Rabbits , Receptors, Adrenergic, alpha/analysisABSTRACT
Hypertonic solutions of different substances were injected into the vertebral artery of dogs anesthetized with chloralose, preventing their access to the hypothalamic osmoreceptors by ligating the basilar artery and both the external carotid arteries. The hypertonic solution of sodium chloride produced graded inhibition of water diuresis and a concomitant rise in plasma antidiuretic hormone (ADH) level; hypertonic solution of glucose produced lesser effect. Hypertonic urea solution, on the other hand, did not alter the course of water diuresis. It was concluded that osmoreceptors are also present in the medulla which sense the changes in blood osmolarity and accordingly modify the ADH release.