Inhibitory actions of tachykinins and neurokinins on release of somatostatin-like immunoreactivity from the isolated perfused rat stomach

• Published in: The Journal of pharmacology and experimental therapeutics Vol. 246; no. 2; pp. 726 - 731
• Main Authors: YIN NAM KWOK, MCINTOSH, C. H. S, SY, H, BROWN, J. C
• Format: Journal Article
• Language: English
• Published: Bethesda, MD American Society for Pharmacology and Experimental Therapeutics 01.08.1988
• Subjects: Animals; Biological and medical sciences; eledoisin; Fundamental and applied biological sciences. Psychology; Gastrins - metabolism; kassinin; Kinins - pharmacology; neurokinin A; neurokinin B; Parasympatholytics - pharmacology; Peptides - metabolism; Rats; Rats, Inbred Strains; somatostatin; Somatostatin - metabolism; Stomach; Stomach - drug effects; Stomach - metabolism; substance P; Substance P - pharmacology; Vertebrates: digestive system; Stomach; Rat; Digestive system; Substance P; Rodentia; Peptide hormone; Kinin; Neuropeptide; Isolated organ; Vertebrata; Mammalia; Immunology; Somatostatin; Tachykinin; Release
• ISSN: 0022-3565; 1521-0103

The present experiments were designed to test the effect of tachykinins and neurokinins on release of somatostatin-like immunoreactivity (SLI) from the isolated perfused stomach. Physalaemin, substance P, kassinin, eledoisin, neurokinin A and neurokinin B inhibited basal SLI release in a dose-dependent manner (1 X 10(-9) to 1 X 10(-7) M). Among all the peptides, physalaemin and substance P were the least potent, whereas kassinin, eledoisin, neurokinin A and B were the more potent compounds in suppressing SLI release. It is proposed that this inhibitory action of tachykinins and neurokinins was mediated by the substance P-K or neurokinin-2 receptor subtype in which kassinin, neurokinin A and eledoisin have been shown to be the more potent agonists. The present study also showed that the effect of neurokinin A, neurokinin B and kassinin was not due to an action involving release of acetylcholine as cholinergic antagonists did not block the SLI inhibitory effect. This suggests that these peptides acted directly on somatostatin containing D-cells.