POSTSYNAPTIC α‐ADRENORECEPTOR POPULATIONS IN SEVERAL VASCULAR SYSTEMS OF THE ANAESTHETIZED RAT

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Abstract
The contribution of postsynaptic .alpha.1- and .alpha.2-adrenoreceptors to vasoconstrictor responses was investigated in several vascular systems of pentobarbital-anesthetized rats pretreated with atropine and propranolol. In the intact circulatory system of the anesthetized rat, pressor responses were obtained to noradrenaline [norepinephrine] 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. The responses to phenylephrine were largely antagonized by prazosin alone. In the blood-perfused hindquarter of the anesthetized rat, a differential blocking activity of prazosin against noradrenaline and phenylephrine was also demonstrated. Prazosin, as observed in the intact circulatory system of the anesthetized rat, was a more potent antagonist against phenylephrine than against noradrenaline. In the blood-perfused mesentery of the anesthetized rat, sympathetic nerve stimulation, noradrenaline and phenylephrine produced a marked vasoconstrictor response while [reserpine] 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. Apparently, the pressor responses to exogenous noradrenaline result from the activation of both postsynaptic .alpha.1- and .alpha.2-adrenoreceptors. The vasoconstrictor responses to neuronally released noradrenaline are largely mediated by activation of postsynaptic .alpha.1-adrenoreceptors. The postsynaptic .alpha.-adrenoreceptor population in the mesenteric resistance blood vessels differs from that in other tissues.