INHIBITION OF GASTRIC MECHANORECEPTOR DISCHARGE BY CHOLECYSTOKININ IN THE RAT

The aim of the present study was to investigate electrophysiologically the effect of systemic cholecystokinin (CCK) on the discharge of vagal gastric mechanoreceptors. Twenty-two single vagal afferent fibers were selected for the investigation of responses to intravenous CCK octapeptide (CCK-8) on the basis of a positive response to gastric distension. Resting discharge in these afferent fibers was 1.3 +/- 0.3 impulses.s(-1) and increased to 9.2 +/- 0.9 impulses.s(-1) during distension (P < 0.0001). CCK (20-100 pmol iv) caused a gastric relaxation of 2.1 +/- 0.2 cmH(2)O and inhibition of phasic motility. The discharge of 20/22 of vagal tension receptors closely followed the magnitude and time course of the fall in pressure. Mean discharge before and after CCK (50 pmol) was 7 +/- 0.9 and 3.9 +/- 0.8 impulses.s(-1), respectively (P < 0.001, n = 22). Both the pressure response and the concomitant changes in afferent discharge were abolished by L-364,718 (1.2 mg/kg iv). Only two afferent units failed to show a decrease in firing following CCK (50 pmol), and at 500 pmol the discharge of these units was augmented. In conclusion, CCK (50 pmol) has predominantly indirect effects on gastric mechanoreceptors, which decrease their firing in association with gastric relaxation.