On the adenosine receptor and adenosine inactivation at the rat diaphragm neuromuscular junction.

摘要: 1. The effects of adenosine and analogues 2-chloroadenosine (CADO), L-N6-phenylisopropyladenosine (L-PIA), D-N6-phenylisopropyladenosine (D-PIA), N6-cyclohexyladenosine (CHA) 5'-N-ethylcarboxamide (NECA) on evoked endplate potentials (e.p.ps) twitch tension were investigated in innervated diaphragms the rat. 2. Adenosine its decreased, a concentration-dependent manner, amplitude both e.p.ps responses by nerve stimulation. order potency decreasing was CHA, L-PIA, NECA greater than D-PIA CADO adenosine. L-PIA about 8 times more potent D-PIA. Neither nor affected directly stimulated tubocurarine-paralysed muscles. 3. 8-Phenyltheophylline (8-PT), theophylline isobutylmethylxanthine (IBMX), concentrations virtually devoid effect neuromuscular transmission, antagonized inhibitory 2-chloroadenosine. alkylxanthines as antagonists receptor at rat diaphragm junction 8-PT IBMX theophylline. antagonism these xanthines shown to be competitive, pA2 value for being 7.16. In slightly higher those used test ability antagonize receptor, increased without modifying their decay phase or resting membrane potential muscle fibre. 4. uptake inhibitor, nitrobenzylthioinosine (NBI) deaminase erythro-9(2-hydroxy-3-nonyl)adenine (EHNA), potentiated junction. potentiation factors 2.6 NBI (5 microM), 2.2 EHNA (25 microM) 4.6 combination microM). 5. It is concluded that deamination contribute inactivation this preparation transmission mediated xanthine-sensitive with an agonist profile which does not fit criteria classification either A1 A2-adenosine receptor.