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. 1995 Oct;116(4):2303–2309. doi: 10.1111/j.1476-5381.1995.tb15069.x

SMS 201-995-induced stimulation of gastric acid secretion via the dorsal vagal complex and inhibition via the hypothalamus in anaesthetized rats.

M Yoneda 1, Y Taché 1
PMCID: PMC1908981  PMID: 8564264

Abstract

1. SMS 201-995, a somatostatin analogue which interacts with highest affinities at somatostatin receptor subtypes 5 > 2 > or = 3, was microinjected into selective brain sites and its influence on pentagastrin (10 micrograms kg-1 h-1, i.v.)-stimulated gastric acid secretion was investigated in rats anaesthetized with urethane. Gastric acid secretion was measured by flushing the stomach with saline through a gastric cannula every 10 min. 2. SMS 201-995 microinjected into the dorsal vagal complex (DVC, 7, 15, 30 and 60 ng) dose-dependently increased pentagastrin-stimulated gastric acid secretion. The peak acid response was reached within 20 min and returned to basal level 50 min post-injection. SMA 201-995 (30 ng) microinjected into the surrounding area or the central amygdala did not modify pentagastrin-stimulated acid secretion. 3. SMS 201-995 injected into the lateral ventricle (i.c.v., 100, 200, or 300 ng), paraventricular nucleus (PVN) or lateral hypothalamus (LH) (7.5, 15, or 30 ng) dose-dependently inhibited pentagastrin-stimulated gastric acid secretion. SMS 201-995 (30 ng) microinjected into the area surrounding the PVN or LH did not modify the acid secretion response to pentagastrin. 4. Vagotomy prevented the effects of SMS 201-995 (30 ng) microinjected into the DVC and LH. 5. Spinal cord transection abolished the inhibitory action of SMS 201-995 (30 ng) microinjected into the PVN but not the LH. 6. These results demonstrate that SMS 201-995 acts in the DVC to enhance and in the LH and PVN to inhibit pentagastrin-stimulated gastric acid secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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