Abstract
The effect of 5′-N-ethylcarboxamidoadenosine (NECA) on rat bronchial smooth muscle was examined in vitro. Both the nerve mediated muscle contraction induced by electrical stimulation and the potassium evoked release of [ 3H]ACh were enhanced by NECA. The apparent affinity (EC 50) of NECA in the contraction experiments was 0.30 ± 0.06 μM. The adenosine (ADO) receptor antagonist, 8-phenyltheophylline (8-PT), inhibited the NECA induced potentiation of both the electrical induced contraction and the potassium evoked release of [ 3H]ACh. The EC 50 and intrinsic activity of exogenous ACh were not altered in the presence of NECA (1 μM) in experiments where smooth muscle contraction were measured, indicating that NECA has a prejunctional effect and not a postjunctional effect on muscarinic receptors. The new A 2 specific ADO receptor agonist 2-p-(2-carboxyethyl)-phenethylamino-5′-N-ethylcarboxamidoadenosine (CGS 21680) and ADO also enhanced the nerve-mediated contraction (EC 50 = 35 ± 8 μM and 69 ± 20 μM, respectively). 8-PT (10 μM) and enprofylline (ENPF) (10 μM) inhibited the electrically induced contraction by 55 ± 16% and 45 ± 5% respectively. The potassium evoked release, however, was stimulated 56 ± 6% and 39 ± 7% by 50 μM 8-PT and ENPF respectively. The results provide evidence for a NECA specific ADO receptor in rat bronchi that is most likely prejunctional. Stimulation of this receptor, which may be of an A 2 receptor subtype, enhances the nerve mediated release of ACh and thereby induce contraction of the bronchial smooth muscle.
Published Version
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