Literature DB >> 9430423

Angiotensin-converting enzyme inhibitors can potentiate ozone-induced airway hyperresponsiveness.

S Matsubara1, H Kikkawa, O Kaminuma, K Ikezawa.   

Abstract

We investigated the effects of single and chronic oral administration of angiotensin-converting enzyme inhibitors on ozone-induced airway hyperresponsiveness in guinea pigs. Ozone exposure (3 ppm for 2 h) significantly increased airway responsiveness in vehicle-treated animals and in animals with either single or chronic administration (8 days) of drugs. Single administration of imidapril, enalapril and captopril significantly potentiated ozone-induced airway hyperresponsiveness at a dose of 100, 50 and 50 mg/kg, respectively, although these doses did not influence airway responsiveness in normal guinea pigs, i.e., the magnitude of potentiation was captopril > enalapril > imidapril. In the study of chronic administration of the drugs, imidapril (10-100 mg/kg per day) had no influence on airway responsiveness in both normal and ozone-treated animals. In contrast, captopril and enalapril (10-100 mg/kg per day) dose-dependently potentiated ozone-induced airway hyperresponsiveness, with no influence on airway responsiveness in normal animals. That is, the magnitude was enalapril > captopril. These results indicate that angiotensin-converting enzyme inhibitors potentiate airway responsiveness in ozone-treated guinea pigs but not in normal guinea pigs and that imidapril is less potent than enalapril and captopril in potentiating ozone-induced airway hyperresponsiveness in guinea pigs.

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Year:  1997        PMID: 9430423     DOI: 10.1016/s0014-2999(97)01316-2

Source DB:  PubMed          Journal:  Eur J Pharmacol        ISSN: 0014-2999            Impact factor:   4.432


  2 in total

1.  Imidapril: will fewer adverse events translate into better long-term outcomes?

Authors:  Tom Richart; Jan A Staessen; Willem H Birkenhäger
Journal:  Drugs       Date:  2007       Impact factor: 9.546

2.  Prevention of airway hyperresponsiveness induced by left ventricular dysfunction in rats.

Authors:  Ferenc Petak; Gergely Albu; Eniko Lele; Maurice Beghetti; Walid Habre
Journal:  Respir Res       Date:  2012-12-13
  2 in total

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