Microinjection of bombesin into the ventrolateral reticular formation inhibits peripherally stimulated gastric acid secretion through spinal pathways in rats.

Bombesin injected into the cisterna magna potently inhibits gastric acid secretion stimulated by intravenous infusion of pentagastrin. Sites in the medulla oblongata where bombesin acts to suppress gastric acid secretion were investigated in urethane-anesthetized rats with gastric cannula. Bombesin or vehicle was injected into the medullary parenchyma or intracisternally (i.c.) 60 min after the start of an intravenous pentagastrin infusion; gastric acid secretion was monitored every 10 min for 20 min before and 150 min after the start of pentagastrin. Bombesin (0.2, 0.6 or 6.2 pmol) microinjected into the ventrolateral reticular formation (VLRF) inhibited dose-dependently the net acid response to pentagastrin by 40.8+/-11.1, 75.4+/-12.8 and 96.7+/-19.4%, respectively, at the 40-50 min period after microinjection compared with the vehicle group. Bombesin action in the VLRF was long lasting (96% inhibition still observed at 90 min after 6.2 pmol), and completely abolished by cervical spinal cord transection at the C6 level. By contrast, bombesin injected i.c. at 0.2 or 0.6 pmol had no effect while at 6.2 pmol, there was a 79.0+/-3.9% peak inhibition of pentagastrin-stimulated acid secretion. Bombesin (6.2 pmol) injected into the dorsal motor nucleus reduced the acid response to pentagastrin by 29%. The parvicellular and gigantocellular reticular nuclei were not responsive to bombesin. These results indicate that bombesin acts in the VLRF to inhibit pentagastrin-stimulated gastric acid secretion through spinal pathways, suggesting a potential role of medullary VLRF area in the sympathetic control of gastric acid secretion.