Purinergic modulation of spontaneous activity and of responses to high potassium and acetylcholine in rat ileal smooth muscle.
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.[1]References
- Purinergic modulation of spontaneous activity and of responses to high potassium and acetylcholine in rat ileal smooth muscle. Mahmod, S.M., Huddart, H. Comp. Biochem. Physiol. C, Comp. Pharmacol. Toxicol. (1993) [Pubmed]
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