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A J Watt

Publications and source records attributed to A J Watt.

27 records · Page 2Linked to original sources

Direct and indirect effects of adenosine 5'-triphosphate on guinea-pig ileum.

1 The inhibitory effects of adenosine 5'-triphosphate (ATP) were compared on the responses to electrical stimulation, and to direct and indirect stimulation by drugs of the longitudinal smooth muscle of guinea-pig ileum before and after blocking nervous activity. 2 While the major inhibitory effect of ATP was an indirect one on the intramural excitatory nerves, there was also a small direct effect on the muscle. 3 ATP also had direct and indirect excitatory effects. The direct effect particularly was only seen with high concentrations of ATP, but the appearance of these excitatory effects may be affected by the inhibitory actions.

Acetylcholine↗

Some mechanism which may modulate noradrenaline release in guinea-pig isolated ileum.

Guinea-pig isolated ileum pre-incubated with [3H]noradrenaline, released 3H-label during coaxial stimulation at 3.2-12.8 Hz. This evoked 3H-overflow seems due to nerve stimulation, and may be frequency-dependent. The 3H-overflow evoked by coaxial stimulation was increased with 2.6 muM phentolamine, reduced at threshold stimulation by 0.56 muM prostaglandin E1, but the tendency for 2.8 muM indomethacin to increase the evoked 3H-overflow was not statistically significant. The results indicate that the release of noradrenaline from guinea-pig ileum may be modulated by activation of presynaptic alpha-adrenoceptors, whereas prostaglandins act mainly at a postsynaptic site to modulate the sympathetic response.

Animals↗

The effect of PGE1 on peristalsis and on perivascular nerve inhibition of peristaltic activity in guinea-pig isolated ileum.

The effect of PGE1 on peristalsis of guinea-pig isolated ileum was examined using a modified Trendelenburg method to evoke and record peristaltic activity. PGE1 (14 nM, 0.11 microM and 0.56 microM) increased peristaltic activity of both longitudinal and circular muscle, mainly by increasing the amplitude of contraction. Preparations of ileum subjected to a 'minimal' peristaltic stimulus were more sensitive to the effects of PGE1 than were preparations subjected to a 'just-maximal' peristaltic stimulus. The inhibition of peristaltic activity caused by perivascular nerve stimulation was antagonized by 0.56 microM PGE1 but slightly increased by 14 nM PGE1.

Animals↗

The effects of adrenaline, noradrenaline and isoprenaline on inhibitory alpha- and beta-adrenoceptors in the longitudinal muscle of the guinea-pig ileum.

1. Two preparations, a segment of the ileum and the myenteric plexuslongitudinal muscle preparation, have been used for an analysis of the inhibitory effects of adrenaline, noradrenaline and isoprenaline on the contractor responses of the longitudinal muscle to acetylcholine or to electrical, coaxial or field, stimulation.2. Since the inhibitory effects of adrenaline, noradrenaline and isoprenaline on the acetylcholine-induced contractions were not affected by phenoxybenzamine but were antagonized by propranolol, it is concluded that beta-adrenoceptors are present on the muscle cells.3. The responses to electrical stimulation were suppressed by adrenaline or noradrenaline but only partly inhibited by isoprenaline. Propranolol antagonized the effect of isoprenaline and, to some extent, that of noradrenaline, but scarcely affected the action of adrenaline. Phenoxybenzamine, on the other hand, antagonized most of the effect of adrenaline and, to some extent, that of noradrenaline; it usually potentiated the effect of isoprenaline.4. The output of acetylcholine evoked by electrical stimulation was diminished by adrenaline or noradrenaline but was not affected by isoprenaline. The depressant effect on acetylcholine release was antagonized by phenoxybenzamine but not affected by propranolol; therefore these effects of adrenaline and noradrenaline are mediated by alpha-adrenoceptors.5. It may be assumed that alpha-adrenoceptors in situ are stimulated mainly by circulating adrenaline and possibly noradrenaline and thus cause a prejunctional inhibition at the nerve-smooth muscle junction.

Acetylcholine↗