Hawthorn M H, Broadley K J, Gibbon C J
Gen Pharmacol. 1985;16(4):371-8. doi: 10.1016/0306-3623(85)90198-3.
beta-Phenylethylamine (PEA) produced a contraction of the guinea-pig isolated lung parenchymal strip and bronchoconstriction of perfused lungs. Reserpine pretreatment had little effect on these responses indicating a substantial direct effect. Phentolamine (10(-6) and 10(-5) M) had minimal effect on PEA in the lung strip compared with that on noradrenaline, eliminating involvement of alpha-adrenoceptors. PEA was unaffected by atropine (10(-7)M) or a mepyramine (10(-7)M); metiamide (10(-4)M) mixture. The contraction was not therefore mediated via muscarinic or histaminergic receptors. 5-HT and dopamine receptors were also discounted. Possible stimulation of a phenylethylaminergic receptor and its relevance to bronchial asthma is discussed.
β-苯乙胺(PEA)可使豚鼠离体肺实质条收缩,并使灌注肺发生支气管收缩。利血平预处理对这些反应影响很小,表明存在实质性的直接作用。与去甲肾上腺素相比,酚妥拉明(10⁻⁶和10⁻⁵M)对肺条中的PEA作用极小,排除了α-肾上腺素能受体的参与。PEA不受阿托品(10⁻⁷M)或美吡拉敏(10⁻⁷M);甲硫咪特(10⁻⁴M)混合物的影响。因此,收缩不是通过毒蕈碱或组胺能受体介导的。5-羟色胺和多巴胺受体也被排除。讨论了苯乙胺能受体的可能刺激及其与支气管哮喘的相关性。