Gastrin and the vagus interact in the trophic control of the rat oxyntic mucosa

Abstract

Gastrin is a trophic hormone for the stomach, and permanent reduction of circulating gastrin by antrectomy leads to atrophy of the oxyntic mucosa, including a reduced density of histamine-storing endocrine cells (so-called ECL cells). Recently, it was proposed that also the vagal nerve has a trophic influence on the stomach. The two vagal trunks innervate the anterior and posterior side of the gastric wall, respectively. This arrangement makes it possible to denervate one side of the stomach selectively. The objective of the present study was to examine the consequences of combined antrectomy and vagotomy (unilateral or bilateral). Male Sprague-Dawley rats were subjected to unilateral or bilateral subdiaphragmatic truncal vagotomy with or without antrectomy. Control rats were sham-operated. The rats were killed 8 weeks after the operation. Bilateral vagotomy raised the basal serum gastrin concentration (fasting level). The thickness of the oxyntic mucosa and the density of ECL cells were not significantly different from age-matched vagally intact controls. Unilateral vagotomy induced no change in the basal serum gastrin concentration, nor did it affect the mucosa on the intact side. On the denervated side, however, there was reduced mucosal thickness and a greatly reduced ECL cell density. With a combination of antrectomy and vagal denervation the decrease in ECL cell density was exaggerated compared to the effect of antrectomy or unilateral vagotomy alone. The results suggest that gastrin and the vagus interact synergistically to maintain the normal integrity of the rat oxyntic mucosa and that the ECL cells represent an important target for both gastrin and the vagus.