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Interaction between alpha2-and beta2-adrenergic receptors in rabbit ciliary processes

 

作者: BausherLarry P.,   GregoryDouglas S.,   SearsMarvin L.,  

 

期刊: Current Eye Research  (Taylor Available online 1987)
卷期: Volume 6, issue 3  

页码: 497-505

 

ISSN:0271-3683

 

年代: 1987

 

DOI:10.3109/02713688709025206

 

出版商: Taylor&Francis

 

数据来源: Taylor

 

摘要:

The interaction between the alpha2- and beta2- adrenergic receptors of ciliary processes has Been studied by examining dose-response curves for adrenergic agonist stimulation of cyclic AMP production by intact, excised rabbit ciliary processes.Stimulation of cyclic AMP production by 1-isoproterenol is maximum from 0.1 to 1.0 uM; at higher concentrations stimulation decreases and approaches basal levels. Decreased cyclic AMP production at high concentrations of isoproterenol is blocked by the specific alpha2-adrenergic antagonist, yohimbine, but not by the alpha1-adrenergic antagonist, prazosin. Ciliary processes from animals after bilateral cervical ganglionectomy also show reduced cyclic AMP production at high concentrations of isoproterenol and this reduction is blocked by yohimbine, but not prazosin. This experiment suggests that the inhibition at high concentrations of isoproterenol is mediated by postsynaptic alpha2-adrenergic receptors. Cyclic AMP production is relatively insensitive to epinephrine and norepinephrine, but their responces are potentiated by yohimbine.Catecholamines and clonidine, a specific alpha2-adrenergic agonist, exhibit dose-dependent inhibition of forskolin-stimulated cyclic AMP production by ciliary processes. I50sfrom the dose-response curves are consistent with the characteristic binding affinities of these adrenergic agonists for alpha2-adrenergic receptors: clonidine = epinephrine>norepinephrine>isoproterenol. Inhibition of forskolin-stimulated cyclic AMP production by clonidine is blocked by yohimbine but not by prazosin.The dose-response curves for catecholamine stimulation of cyclic AMP production can be understood in terms of the relative affinities of these adrenergic agonists for beta2- and alpha2-adrenergic receptors linked to adenylate cyclase via N and Nirespectively. The interaction between these two adrenergic receptors, one which stimulates and one which inhibits stimulation of adenylate cyclase may provide an explanation for some of the paradoxical observations from studies of the effects of catecholamines on aqueous flow.

 

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