Mechanism of action of somatostatin on the canine ileal circular muscle.

The aim of this study was to investigate the mechanism of action of somatostatin on the circular muscle of the isolated canine ileum using the microelectrode technique. The membrane potential from circular muscle cells was recorded in two preparations: 1) whole thickness circular and longitudinal muscle (with intact myenteric and deep muscular plexuses, n = 13) and 2) isolated circular muscle (with only deep muscular plexus, n = 9). In this preparation, inhibitory junction potentials (IJPs), elicited after field stimulation, are mediated by a nitric oxide-related (NO-R) compound. Somatostatin (10(-6) M) transiently (2-5 min) depolarized the circular muscle cells in both whole thickness (3.6 +/- 1.0 mV, P < 0.01) and isolated circular muscle preparations (8.0 +/- 0.8 mV, P < 0.01). Somatostatin did not reduce either the amplitude or duration of the IJP in the isolated circular muscle but reduced slow-wave amplitude. In contrast, a reduction (20-50%) in the amplitude of the IJP was observed in the whole thickness preparation, and there was little effect on slow-wave amplitude. Somatostatin did not affect the induced slow wave observed in the whole thickness preparation after field stimulation. Apamin significantly reduced the amplitude of the IJP in both preparations. Somatostatin (10(-6) M) did not modify the apamin-resistant IJP. A reduction in the slow-wave amplitude was observed in the isolated circular muscle preparation.(ABSTRACT TRUNCATED AT 250 WORDS)