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    Hypophagic effect of the angiotensin AT1 receptor antagonist irbesartan in rats (2007)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Voigt, Jörg-Peter
    Bramlage, Peter
    Fink, Heidrun
    Quelle
    European journal of pharmacology; 564(1/3) — S. 131–137
    ISSN: 1879-0712
    Sprache
    Englisch
    Verweise
    Pubmed: 17408613
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    +49 30 838 53221
    pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Recent experimental and clinical studies report beneficial metabolic effects of antihypertensive drugs interfering with angiotensin. Antagonists at the angiotensin AT(1) receptor can reduce blood glucose and triglyceride levels. So far, there is little evidence, however, that angiotensin AT(1) receptor antagonists can also affect food intake. Particularly unknown is if drugs of this class can have acute effects on short term feeding. To address this issue, the angiotensin AT(1) receptor antagonist irbesartan was studied in a one-hour feeding paradigm in rats. In this study, irbesartan was investigated in comparison with fenfluramine, an established satiating drug, and the angiotensin converting enzyme (ACE) inhibitor captopril. We found a significant reduction of one-hour food intake following 100-200 mg/kg (i.p.) irbesartan. The ACE inhibitor captopril (25-100 mg/kg i.p.) remained without effect on food intake and fenfluramine showed the expected hypophagic action starting at 1 mg/kg (i.p.). The hypophagic effect of irbesartan could not be attributed to sedation or any gross effect on motor activity as determined both upon feeding and independent activity experiments. Fenfluramine (1 mg/kg) and irbesartan (100 mg/kg) did not reduce the latency to feed, but similarly reduced the eating rate at the beginning of the test meal. In conclusion, the present study demonstrates a hypophagic effect of the angiotensin AT(1) receptor antagonist irbesartan that cannot be attributed to sedation or antidipsic effects of the drug.