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[Central mechanism of inhibitory effect of histamine H1-receptor agonists PEA on gastric acid secretion].

The present experiment is undertaken to study the central mechanism of the inhibitory effect of 2-pyridylethylamine (PEA, i.c.v.) on the gastric acid secretion. Gastric acid was continuously washed out with 37 degrees C saline by means of a perfusion pump in male adrenalectomized wistar rats. Drugs were injected into the third ventricle to examine the effect on pentagastrin-induced (160 micrograms/kg, s.c.) gastric acid secretion. The results were as follows: (1) Pretreatment with CRF-antiserum (2.5 microliters, 1:20,000, i.c.v.) blocked the inhibitory effect of PEA (10 micrograms, i.c.v.) on gastric acid secretion. (2) Administration of CRF (1 and 2 micrograms, i.c.v.) or beta-endorphin (0.94 and 1.25 micrograms, i.c.v.) markedly inhibited the gastric acid secretion. (3) Pretreatment with naloxone (5 micrograms, i.c.v.) blocked the inhibitory effect of CRF (1 microgram, i.c.v.), but the inhibitory effect of beta-endorphin (0.94 microgram, i.c.v.) was not changed by pretreatment with CRF-antiserum (1:20,000, 2.5 microliters, i.c.v.). These results suggest that PEA stimulates the release of hypothalamic CRF which stimulates the release of hypothalamic endogenous opioid peptides. The peptides again induces vagus nerve-mediated inhibitory effect on gastric acid sceretion.