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Effect of ambrein on smooth muscle responses to various agonists
Institution:1. Laboratório de Microscopia Celular e Tecidual, Programa de Pós-graduação em Biologia Estrutural e Funcional, Departamento de Morfologia, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil;2. Departamento de Ciências Morfofisiológicas, Universidade Estadual de Maringá, Maringá, PR, Brazil;3. Faculdade de Medicina Veterinária, Centro Universitário Monte Serrat (UNIMONTE), Santos, São Paulo, Brazil;4. Laboratório de Histologia, Departamento de Morfologia, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil;5. Departamento de Anatomia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brazil;6. Universidade Federal do Piauí, Campus Senador Helvídio Nunes de Barros, Picos, PI, Brazil
Abstract:The pharmacological effects of ambrein (isolated from ambergris) on the contractile responses induced by some agonists in smooth muscle preparations were investigated. Ambrein in the concentration range of 10, 50 and 250 μg/ml decreased the spontaneous contraction of the isolated rabbit jejunum, rat uterus and guinea-pig vas deferens. Ambrein-induced antagonism to acetylcholine (Ach) in the guinea-pig ileum was abolished when the concentration of calcium chloride in the Tyrode's solution was increased to 5 mM/l. Furthermore, ambrein did not antagonise nicotine-induced contractions in the isolated rabbit jejunum or serotonin-induced contractions in the isolated guinea-pig ileum and vas deferens or the rat uterus. However, ambrein in the concentration range of 10, 50 and 250 μg/ml antagonised prostaglandins (PGs) E2, D2, F2α, and oxytocin-induced contractions in the rat uterus in vitro. Ambrein also antagonised (±) noradrenaline and (?) adrenaline-induced contractions in the isolated guinea-pig vas deferens. It is concluded that ambrein-induced non-selective dose-dependent antagonism to the effects of some agonists (Ach, adrenaline, noradrenaline, PGs and oxytocin) in some smooth muscles may be due to the ability of this compound to interfere with the mobilisation of extracellular Ca2+ required for muscular contractions induced by these agonists.
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