Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[Central mechanism of inhibitory effect of histamine H1-receptor agonists PEA on gastric acid secretion]. 757 Jan 11

Murine thymocytes activated with the mitogen Con A express proenkephalin A mRNA (PEA mRNA) and met-enkephalin and/or met-enkephalin-containing peptides ("enkephalins"). This Con A-induced expression of PEA mRNA is modulated by the delta opioid receptor agonist, deltorphin I, in a biphasic, dose-dependent manner. That is, 10(-13) M to 10(-11) M deltorphin enhanced PEA mRNA expression 3- to 3.5-fold over the level induced by Con A alone, and 10(-9) M to 10(-7) M deltorphin inhibited it 40 to 70%. delta opioid receptor antagonists recognizing the delta-2 (naltrindole (NTI) and naltriben (NTB)), but not the delta-1 (7-benzylidenenaltrexone (BNTX)), subtype of opioid receptor described in brain, reversed both the enhancing and inhibiting effects of deltorphin on Con A-induced PEA mRNA expression. In addition, the delta-2 receptor-specific antagonists, NTI and NTB, directly inhibited Con A-induced PEA mRNA expression. The function of the enkephalins expressed by thymocytes was examined by using 1) delta opioid receptor antagonists, 2) PEA mRNA-specific antisense cDNA, and 3) Ab to met-enkephalin, and measuring cell proliferation. All three reagents caused enhancement of Con A-induced proliferation, with effects ranging from two- to fourfold over the response to Con A alone. Again, the delta-2 subtype-specific antagonists, NTI and NTB, were functional and the delta-1 subtype-specific antagonist, BNTX, was not. The PEA mRNA-specific antisense cDNA blocked translation but not transcription of PEA mRNA. The data suggest that 1) endogenous enkephalins induced in thymocytes modulate their own expression through delta-2-like opioid receptors, and 2) these endogenous enkephalins function to inhibit the proliferation of activated thymocytes.
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PMID:Met-enkephalin-containing peptides encoded by proenkephalin A mRNA expressed in activated murine thymocytes inhibit thymocyte proliferation. 773 Jun 11