Sm. Mahmod et H. Huddart, PURINERGIC MODULATION OF SPONTANEOUS ACTIVITY AND OF RESPONSES TO HIGH POTASSIUM AND ACETYLCHOLINE IN RAT ILEAL SMOOTH-MUSCLE, Comparative biochemistry and physiology. C. Comparative pharmacologyand toxicology, 106(1), 1993, pp. 79-85
1. In rat ileal smooth muscle both adenosine and ATP at 10(-4) M signi
ficantly enhanced spontaneous mechanical activity. The excitatory acti
ons of adenosine were blocked by the P1 receptor antagonist 8-phenylth
eophylline and the excitatory effects of ATP were significantly reduce
d by the P2 receptor antagonist quinidine. 2. The P2 receptor desensit
izer alpha,beta-methylene-ATP was without effect on ACh responses nor
did the stable analogue beta,gamma-methylene-ATP exert any effect on s
pontaneous mechanical activity. 3. Pretreatment with adenosine caused
a dose-dependent enhancement of K-induced contractures in the ileum. L
ow adenosine concentrations slightly inhibited and high concentrations
slightly enhanced ACh-induced contractures in the ileum. 4. ATP poten
tiated the phasic component of the ileal K-induced contracture but str
ongly inhibited tonic force at high concentrations. This agent slightl
y inhibited the phasic component of the ACh-induced contracture while
strongly inhibiting ACh-induced tonic force. 5. Alpha,beta-methylene-A
TP inhibited ileal muscle ACh induced contractures while it potentiate
d both phasic and tonic K-induced contractures. Beta,gamma-methylene A
TP inhibited ACh-induced contractures but it enhanced K-induced phasic
contractures while inhibiting K-induced tonic force. 6. The results o
f 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 inte
ractions with ileal smooth muscle may inactivate slow voltage-dependen
t calcium channels leading to EC uncoupling.