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Purinergic modulation of spontaneous activity and of responses to high potassium and acetylcholine in rat ileal smooth muscle.

Research output: Contribution to journalJournal article

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  • S. M. Mahmod
  • H. Huddart
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<mark>Journal publication date</mark>1993
<mark>Journal</mark>Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology
Issue number1
Volume106
Number of pages7
Pages (from-to)79-85
Publication StatusPublished
<mark>Original language</mark>English

Abstract

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 α,β-methylene-ATP was without effect on ACh responses nor did the stable analogue β,gg-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. α,β-methylene-ATP inhibited ileal muscle ACh induced contractures while it potentiated both phasic and tonic K-induced contractures. β, γ-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.