Reversal by prostaglandin E2 of the inhibitory effect of indomethacin on contractions of guinea-pig ileum induced by angiotensin

Inhibition of Peristalsis in Guinea‐pig Isolated Ileum and Colon by Drugs That Block Prostaglandin Synthesis

“…Inhibition by serosally applied aspirin was lost or reduced after addition of prostaglandin E2 (Bennett et al, 1975b) indicate that indomethacin at concentrations up to 3.6 jg/ml had no significant effect on contractions of the longitudinal muscle induced by ACh, and caused at most a small depression of contractions to electrical field stimulation at 4 Hz. However, indomethacin 20 jg/ml (Chong & Downing, 1974) or 40 gg/ml (Bennett et al, 1975b) caused non-selective depression. The present experiments indicate a small inhibitory effect of indomethacin 1-4 jg/ml on responses to nicotine, a greater inhibition of responses to prostaglandin E2, but no effect on those to ACh.…”

“…However, indomethacin 20 jg/ml (Chong & Downing, 1974) or 40 gg/ml (Bennett et al, 1975b) caused non-selective depression. (Ambache et al, 1966).…”

“…These results suggest that prostaglandins may be involved in peristalsis. Furthermore, prostaglandin E may modulate the response to cholinergic nerve stimulation (Ehrenpreis, Greenberg & Belman, 1973;Chong & Downing, 1974;Kadlec, Masek & geferna, 1974;Bennett et al, 1975b). We therefore studied the effects of drugs which inhibit prostaglandin synthesis (Ferreira, Moncada & Vane, 1971;Smith & Willis, 1971;Vane, 1971) on peristaltic activity in guinea-pig isolated ileum and colon.…”

Basic Mechanisms of Prostaglandin Action on Autonomic Neurotransmission

“…Thus, PGE, and PGE2 enhance the contraction response to cholinergic nerve stimulation in guinea pig and rabbit ileum (51, 134, 144-146), while the effects on contractions induced by ACh are less clear; both enhanced and unchanged responses have been reported (51, 144). On the other hand, contraction responses to nerve stimulation or administration of angiotensin (a substance which partly acts by releasing ACh) are markedly reduced or almost abolished by indomethacin, and partially or com pletely restored by subsequent administration of small, subspasmogenic doses of PGE, and PGE2 (134,144,(147)(148)(149)(150). The contraction response to ACh seems to be little affected by indomethacin (144,151).…”

PROSTAGLANDIN ANTAGONISM BY SODIUM p‐BENZYL‐4‐[1‐OXO‐2‐(4‐CHLOROBENZYL)‐3‐PHENYLPROPYL]PHENYL PHOSPHONATE (N‐O164)

“…The reason for this is not immediately apparent. The reduction of contractions produced by 5-hydroxytryptamine on the rat stomach strip and angiotensin and bradykinin on the gerbil colon by N-0164 in the present experiments may reflect a degree of involvement of prostaglandins in contractions produced by these substances (Chong & Downing, 1974;Frankhuijzen & Bonta, 1975;Crocker & Willavoys, 1976) but a definitive conclusion must await further investigation. However, it is interesting to note that although the dose-ratios for prostaglandin E2 and FM increased with increasing concentrations of N-0164, the dose-ratio for 5-hydroxytryptamine increased a certain amount and then remained unaltered when the concentration of N-0164 was approximately doubled.…”