1. In rat ileal smooth muscle both
adenosine and
ATP at 10(-4) M significantly enhanced spontaneous mechanical activity. The excitatory actions of
adenosine were blocked by the P1 receptor antagonist
8-phenyltheophylline and the excitatory effects of
ATP were significantly reduced by the P2 receptor antagonist
quinidine. 2. The P2 receptor desensitizer
alpha,beta-methylene-ATP was without effect on ACh responses nor did the stable analogue
beta,gamma-methylene-ATP exert any effect on spontaneous mechanical activity. 3. Pretreatment with
adenosine caused a dose-dependent enhancement of K-induced
contractures in the ileum. Low
adenosine concentrations slightly inhibited and high concentrations slightly enhanced ACh-induced
contractures in the ileum. 4.
ATP potentiated the phasic component of the ileal K-induced
contracture but strongly inhibited tonic force at high concentrations. This agent slightly inhibited the phasic component of the ACh-induced
contracture while strongly inhibiting ACh-induced tonic force. 5.
alpha,beta-methylene-ATP inhibited ileal muscle ACh induced
contractures while it potentiated both phasic and tonic K-induced
contractures.
beta,gamma-methylene ATP inhibited ACh-induced
contractures but it enhanced K-induced phasic
contractures while inhibiting K-induced tonic force. 6. The results of this study suggest that rat ileum may contain the A1 subtype of the P1 receptor but the evidence for a P2 receptor subtype is conflicting despite the inhibition of
ATP actions by
quinidine. 7. The inhibition of K- and ACh-induced tonic force suggests that
adenosine and
ATP interactions with ileal smooth muscle may inactivate slow
voltage-dependent calcium channels leading to EC uncoupling.