期刊
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY
卷 54, 期 6, 页码 622-626出版社
WILEY
DOI: 10.1046/j.1365-2125.2002.t01-4-01689.x
关键词
angiotensin II type 1 receptor; angiotensin II; asthma; bronchial hyper-responsiveness; candesartan cilexetil; methacholine
Aims Angiotensin II is a putative mediator in bronchial asthma. There have been very few studies investigating the involvement of angiotensin II receptors in bronchial hyper-responsiveness in asthmatic patients. We examined the effect of candesartan cilexetil, a specific angiotensin II type 1 (AT1) receptor antagonist, on bronchial responsiveness to inhaled methacholine in patients with asthma. Methods Bronchial responsiveness to methacholine, assessed as the concentration of methacholine producing a 20% fall in FEV1 (PC (20) -FEV1 ), was measured on three occasions 2 weeks apart in 11 stable asthmatic patients. Candesartan cilexetil (8 mg once a day) or a placebo was orally administered for 1 week before the methacholine provocation test in a double-blind, randomized, crossover manner. Results Although there were no significant differences between treatment periods in FEV1 values at baseline, the geometric mean (95% CI) PC (20) -FEV1 values increased significantly (P = 0.041) from 0.691 (0.379, 1.259) mg ml(-1) with placebo to 0.837 (0.506, 1.384) mg ml(-1) with candesartan. Candesartan decreased the mean (95% CI) arterial blood pressure (placebo: 95.6 (89.0, 102.2) mmHg, candesartan: 86.4 (79.8, 93.1) mmHg, P = 0.015). There was no correlation between the change in blood pressure and the change in PC (20) -FEV1 . Conclusions We conclude that AT1 receptors are involved in bronchial hyper-responsiveness in asthmatic patients.
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