Interleukin-1 inhibits drinking behaviour through prostaglandins, but not by nitric oxide formation
| Autor: | Gioacchino Calapai, Luca Parente, Maria C. Marciano, Gabriella Facciolà, Achille P. Caputi, Felice Nava |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Nitric oxide formation Dose dependence Drinking Behavior Nitric Oxide General Biochemistry Genetics and Molecular Biology Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Internal medicine medicine Animals Enzyme Inhibitors General Pharmacology Toxicology and Pharmaceutics Injections Intraventricular Drinking behaviour Aspirin biology Interleukin General Medicine Angiotensin II Rats Preoptic area Nitric oxide synthase NG-Nitroarginine Methyl Ester Endocrinology chemistry Prostaglandins biology.protein Nitric Oxide Synthase Interleukin-1 |
| Popis: | Interleukin-1 beta (IL-1 beta) causes inhibition of drinking behaviour. Moreover it induces formation of prostaglandins (PGs) and nitric oxide (NO). Both PGs and NO are able to inhibit drinking stimulated by water deprivation or by intracerebroventricular (i.c.v.) administration of angiotensin II. In this study, we studied in the preoptic area (POA) the possible role of PGs and NO in the antidipsogenic action induced by IL-1 beta. IL-1 beta was injected in the lateral cerebral ventricle (i.c.v.) (2.5, 10, 20, and 40 ng/rat) or into POA (0.625, 1.25, 2.5, and 10 ng/rat). L-arginine (12.5, 25, 50, and 100 ng/rat), the precursor of NO, or NG-nitro-L-arginine methyl ester (L-NAME) (25, 50, and 100 ng/rat), an inhibitor of nitric oxide synthase (NOS), were injected only into POA. Drinking behaviour was induced by water deprivation (24 h). IL-1 beta injected either i.c.v. or into POA caused dose dependent inhibition of drinking. In the POA a treatment with acetylsalicylic acid (ASA) (33, 66, and 135 micrograms/rat), but not with L-NAME, antagonized the inhibition of drinking behaviour induced by the highest doses of IL-1 beta in the POA. In the POA, a treatment with ASA or L-NAME antagonized the inhibition of drinking behaviour caused by injection of the highest doses of L-arginine. Our data suggest that the central inhibition of drinking behaviour of IL-1 beta is mediated through the formation of PGs, but not NO, in the POA. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|