Postsynaptic alpha-adrenoreceptor populations in several vascular systems of the anaesthetized rat.

The contribution of postsynaptic alpha 1- and alpha 2-adrenoreceptors to vasoconstrictor responses was investigated in several vascular systems of pentobarbital-anaesthetized rats pretreated with atropine and propranolol. In the intact circulatory system of the anaesthetized rat, pressor responses were obtained to noradrenaline and phenylephrine. The pressor responses to noradrenaline were only partially blocked by prazosin and the responses which remained after prazosin were significantly reduced further by the subsequent addition of yohimbine. However, the responses to phenylephrine were largely antagonized by prazosin alone. In the blood-perfused hindquarter of the anaesthetized rat, a differential blocking activity of prazosin against noradrenaline and phenylephrine was also demonstrated. Prazosin, as observed in the intact circulatory system of the anaesthetized rat, was a more potent antagonist against phenylephrine than against noradrenaline. In the blood-perfused mesentery of the anaesthetized rat, sympathetic nerve stimulation, noradrenaline and phenylephrine produced a marked vasoconstrictor response whilst B-HT 920 hardly induced a pressor response. The pressor responses to nerve stimulation, noradrenaline and phenylephrine were largely blocked by prazosin alone. However, only the responses to all frequencies of nerve stimulation were enhanced by yohimbine pretreatment. These results obtained from the intact animal and blood-perfused hindquarter indicate that the pressor responses to exogenous noradrenaline result from the activation of both postsynaptic alpha 1- and alpha 2- adrenoreceptors. However, the result obtained from the blood-perfused mesentery indicates that the vasoconstrictor responses to neuronally released noradrenaline are largely mediated by activation of postsynaptic alpha 1-adrenoreceptors. Consequently, these results suggest that, in rats, the postsynaptic alpha-adrenoreceptor population in the mesenteric resistance blood vessels differs from that in other tissues.