Characterization of alpha-adrenoceptors involved in central thermoregulation in rabbits.

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.

Effects of Various alpha-Adrenoceptor Antagonists on Pressor Responses to Norepinephrine and Phenylephrine / 대한마취과학회지

1) The effects of various alpha-adrenoceptor antagonists on the pressor responses to norepinephrine and phenylephrine were examined in anesthetized rabbits in an attempt to determine whether alpha1 and alpha2-adrenoceptors are located on vascular smooth muscle. 2) yohimbine and piperoxan caused a much greater reduction in the pressor responses(rise of 30~50mmHg) to norepinephrine than to phenylephrine, where as labetalol, thymoxamine, phentolamine and prazosin showed a much greater selectively in reducing the pressor responses to phnylephrine than to norepinephrine. 3) The prssor action of small dose of norepinephrine(rise of 10~20mmHg) was not significantly inhibited by the doses of labetalol, thymoxamine and prazosin which caused marked reduction of the above phenylephrine pressor responses, but yohimbine, piperoxan and phentolamine weakend the action significantly. 4) The results suggest that there are two types, alpha 1 and alpha 2, of postsynaptic alpha-adrenoceptors in the vasculature of rabbits. It seems that phenylephrine produces pressor responses by acting alpha 1-type adrenoreceptors: small doses of norepinephrine by acting on alpha 2-type: large doses of norepinephrine by acting on both types.

The Relationship Between Increased Intracranial Pressure and Central alpha-Adrenoceptors

The author attempted to clarify the nature of alpha-adrenoceptors in relation to the pressor response to the increased intracranial pressure(ICP) in urethane-anesthetized rabbits, using the epidural balloon method. 1) The blood pressure increased in parallel with the raised ICP which was made by gradual inflation of the balloon. 2) B-HT 920, an alpha2-agonist, which elicited depressor and bradycardiac responses in normal rabbits inhibited markedly the pressor response to the raised ICP. 3) Piperoxan, an alpha2-antagonist, potentiated the pressor response to the raised ICP. 4) Piperoxan antagonized the depressor and bradycardiac responses by B-HT 920 as well as the inhibitory effect of B-HT 920 on the pressor response to the raised ICP. 5) The pressor response to the raised ICP were not affected at all by prazosin, an alpha1-antagonist. 6) Neither the depressor and bradycardiac responses by B-HT 920 itself nor the inhibitory effect of B-HT 920 on the pressor response to the raised ICP were significantly affected by prazosin. It is inferred from these observations that the central alpha-adrenoceptors play an important role in producing the pressor response to the raised ICP and that the receptors involved here seems to be of alpha2-type.

The Relationship Between Increased Intracranial Pressure and Central alpha-Adrenoceptors

The author attempted to clarify the nature of alpha-adrenoceptors in relation to the pressor response to the increased intracranial pressure(ICP) in urethane-anesthetized rabbits, using the epidural balloon method. 1) The blood pressure increased in parallel with the raised ICP which was made by gradual inflation of the balloon. 2) B-HT 920, an alpha2-agonist, which elicited depressor and bradycardiac responses in normal rabbits inhibited markedly the pressor response to the raised ICP. 3) Piperoxan, an alpha2-antagonist, potentiated the pressor response to the raised ICP. 4) Piperoxan antagonized the depressor and bradycardiac responses by B-HT 920 as well as the inhibitory effect of B-HT 920 on the pressor response to the raised ICP. 5) The pressor response to the raised ICP were not affected at all by prazosin, an alpha1-antagonist. 6) Neither the depressor and bradycardiac responses by B-HT 920 itself nor the inhibitory effect of B-HT 920 on the pressor response to the raised ICP were significantly affected by prazosin. It is inferred from these observations that the central alpha-adrenoceptors play an important role in producing the pressor response to the raised ICP and that the receptors involved here seems to be of alpha2-type.

Central histaminoceptor-adrenoceptor interrelations in the release of adrenocorticotrophic hormone.

Intracerebroventricular administration of adrenaline, noradrenaline phenylephrine, clonidine and histamine produced a significant rise in plasma cortisol concentration whereas isoprenaline had no effect. alpha-Adrenoceptor blockers (yohimbine or piperoxon) per se did not alter the plasma cortisol level. Central pretreatment with yohimbine or piperoxin, blocked the rise in plasma cortisol level induced by icv noradrenaline, phenylephrine and clonidine. In another set of experiments, both H1 and H2 receptor antagonists (mepyramine, and metiamide) per se had not significant effect on plasma cortisol concentration. Central histamine induced rise in plasma cortisol concentration was significantly blocked by icv pretreatment with both H1 and H2 receptor blockers. Furthermore, yohimbine also significantly prevented the rise of plasma cortisol level induced by icv histamine.