Benazepril, an angiotensin converting enzyme inhibitor: drug interaction with salbutamol and bronchial response to histamine in normal subjects

Abstract

Aims To investigate the effect of the angiotensin converting enzyme inhibitor, benazepril, on pulmonary function. Methods We investigated the influence of benazepril, on lung function and the interaction with inhaled salbutamol (0.1 to 6.6 mg ) and histamine (0.03 to 30.69 g l −1 ) in normal subjects. Benazepril 20 mg, salbutamol 8 mg, propranolol 160 mg, and placebo were given orally once daily over 10 days.Results On day 8, there was no difference in the area under the salbutamol doseresponse curves between benazepril, placebo and oral salbutamol ( P >0.05), propranolol shifted the curves to the right ( P<0.05). On day 10, histamine challenge resulted in following PD 35 sGaw values (geometric mean and 95% CI): with placebo 1.02 (0.95-1.09) g l −1 , benazepril 1.04 (0.99-1.08), salbutamol 1.19(1.13-1.25), propranolol 0.57 (0.50-0.65).Conclusions Benazepril had no influence on baseline lung function, caused no interaction with inhaled salbutamol and the bronchial response to histamine was similar to placebo. However, our findings in normal subjects cannot be extrapolated automatically to asthmatics.

The effect of angiotensin-converting enzyme inhibition by captopril on respiratory mechanics in healthy rats

“…However, the authors of the latter used clinically hypotensive low dosages of ACE inhibitors different from captopril 9,10 , or tested much lower captopril dosages 11 . By applying the end-inflation occlusion method, we have been able also to measure the overall inflation inspiratory pressure dissipation including the viscoelastic effects due to stress relaxation.…”

“…However, Jamison and Glover 9 observed no effect of ACE inhibition either on basal airway mechanics or on hypocapnic hyperventilation-induced bronchoconstriction in normal subjects. Moreover, ACE inhibition has been demonstrated to leave unaltered baseline lung function in normal subjects 10 , and basal airway resistance and bradychinine-induced bronchoconstriction in guinea pigs 11 . Type 1 angiotensin receptor antagonism did not alter airway resistance in normal guinea pigs 7 .…”