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首页> 外文期刊>Pigment cell research >Coexistence of β1‐ and β2‐Adrenoceptors in the Melanophore of the GobyTridentiger obscurus*
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Coexistence of β1‐ and β2‐Adrenoceptors in the Melanophore of the GobyTridentiger obscurus*

机译:Coexistence of β1‐ and β2‐Adrenoceptors in the Melanophore of the GobyTridentiger obscurus*

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The effects of β‐adrenergic agonists and antagonists on the pigmentary state of denervated melanophores in isolated, split, caudal fins of the gobyTridentiger obscuruswere examined to investigate the function and the subtype of the β‐adrenoceptors of the melanophores. Salbutamol, terbutaline, and dobutamine partially inhibited the pigment‐aggregating response of melanophores to norepinephrine. The effects of these β‐agonists were inhibited by propranolol. It was confirmed that the melanophores possess both α‐and β‐adrenoceptors, and that the activation of the β‐adrenoceptors induces the dispersion of pigment in the melanophores. Norepinephrine, epinephrine, isoproterenol, dobutamine, salbutamol, and terbutaline evoked the dispersion of pigment in the melanophores in which pigment had previously been aggregated by treatment with verapamil in the presence of phentolamine. The pigment‐dispersing effects of two β1‐selective agonists, norepinephrine and dobutamine, were effectively inhibited by metoprolol, a selective antagonist of β1‐receptors. By contrast, the pigment‐dispersing effects of two β2‐selective agonists, salbutamol and terbutaline, were not inhibited by metoprolol. Both the effects of nonselective agonists, epinephrine and isoproterenol, were partially inhibited by metoprolol. The actions of all of the β‐agonists used were effectively inhibited by propranolol, and they were partially inhibited by butoxamine. These results suggest coexistence of β1‐ and β2‐adrenoceptors in the melanophores. The relative numbers of β1‐ and β2‐adrenoreceptors as a percentage of the total population of β‐adrenoceptors were estimated to be 18.6 and 81.4, respectively, from analyses of Hofstee plots of the effects of the β‐agonists on the mel

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