Summary1. 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 3-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 a-adrenoceptors. 5. It may be assumed that a-adrenoceptors in situ are stimulated mainly by circulating adrenaline and possibly noradrenaline and thus cause a prejunctional inhibition at the nerve-smooth muscle junction.

Summary1. In a preparation consisting of the myenteric plexus and the longitudinal muscle layer removed from a segment of guinea-pig ileum, spontaneous action potentials occurred which were unaffected by tetrodotoxin but suppressed by Mn2+ and were therefore myogenic. 2. A single current pulse of 0-1 ms duration evoked a response consisting of an early action potential followed after a delay of about 200 ms by a complex of biphasic spikes. The first action potential was conducted for no more than 15 mm and the second complex for 30-70 mm.3. Since the first action potential was unaffected by hyoscine or Mn2" but abolished by tetrodotoxin, it was due to excitation of nerve fibres. The later complex of spikes was suppressed by hyoscine and Mn2+ and therefore due to excitation of smooth muscle. It was also inhibited by adrenaline or morphine, compounds which depress acetylcholine release. The evoked smooth muscle response was followed by absence of spontaneous electrical activity for 2-4 seconds. 4. The nerves travelling in a longitudinal direction had a mean maximum conduction velocity of 0 65 m/s, an absolute refractory period of 2-8 ms and a relative refractory period of about 20 ms. 5. The conduction velocity of the smooth muscle response evoked by stimulation of the nerve with a single pulse was 0-16 m/second. After a single pulse the muscle was inexcitable for 0-7-1 3 s; the delay of transmission from nerve to muscle was 210 ms. When instead of a single pulse a train of two-five pulses at 20 ms intervals was applied, the size, conduction distance and con-

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