Effects of peptide hormones in urate crystal inflammation.
Effects of hormonal peptides on inflammation were investigated in normal rats receiving injections of urate crystals into the hindpaw. Beta endorphin, somatostatin and alpha melanocyte stimulating hormone injected along with urate crystals produced diminished swelling. Neurotensin and substance P produced increased swelling. Intramuscular calcitonin inhibited inflammation. In rats made deficient in essential fatty acids, thereby becoming deficient in prostaglandins, beta endorphin nullified the proinflammogenic activity of prostaglandin E2. A hypothesis is proposed that modification of inflammation by neuropeptides is part of the continuum of inflammation-regeneration, a generalized host defense mechanism against noxious stimuli.
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Denko
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Gabriel
D000818:Animals; D002116:Calcitonin / Q000494:pharmacology; D015232:Dinoprostone; D004723:Endorphins / Q000494:pharmacology; D005228:Fatty Acids, Essential / Q000172:deficiency; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology*; D008297:Male; D009074:Melanocyte-Stimulating Hormones / Q000494:pharmacology; D009496:Neurotensin / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000494:pharmacology; D013373:Substance P / Q000494:pharmacology; D014527:Uric Acid / Q000494:pharmacology*; D001615:beta-Endorphin
D004723:Endorphins; D005228:Fatty Acids, Essential; D010455:Peptides; D011458:Prostaglandins E; D014527:Uric Acid; D013373:Substance P; D009496:Neurotensin; D013004:Somatostatin; D001615:beta-Endorphin; D009074:Melanocyte-Stimulating Hormones; D002116:Calcitonin; D015232:Dinoprostone