Increased cough reflex associated with angiotensin converting enzyme inhibitor cough.

Fuller, R W; Choudry, N B

doi:10.1136/bmj.295.6605.1025-a

Cited by 114 publications

(56 citation statements)

References 4 publications

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“…These observations could be of relevance to the cough induced by ACE inhibitors (Fuller & Choudry, 1987) since, if ACE is involved in the degradation of BK in the respiratory tract, then any inhibition of this enzyme may potentiate the action of BK on sensory nerves in the respiratory tract, and thus lead to a lowered cough threshold.…”

Section: Discussionmentioning

confidence: 99%

The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

Ichinose¹,

Barnes²

1990

British J Pharmacology

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1 Bradykinin (BK) instilled directly into the airway lumen caused bronchoconstriction in anaesthetized, mechanically ventilated guinea-pigs in the presence of propranolol (1 mg kg-i.v.) The geometric mean dose of BK required to produce 100% increase in airway opening pressure (PD100) was 22.9 nmol (95% c.i. 11.7-44.6 nmol). 2 The dose-response curve for the effect of instilled BK was significantly shifted to the left by the angiotensin converting enzyme (ACE) inhibitor, captopril (5 and 50nmol instillation, PD100 = 3.0, 95% c.i. 0.98-8.9, and 2.0 nmol, 95% ci. 0.65-6.2 nmol, respectively). 3 The neutral endopeptidase (NEP) inhibitor, phosphoramidon (5 and 50nmol instillation) also shifted the dose-response curve for the effect of instilled BK; the PD100 values = 2.2 (95% c.i. 0.40-11.7) and 1.8 nmol (95% c.i. 0.87-3.5 nmol), respectively. 4 After pretreatment with captopril (50nmol) and phosphoramidon (50nmol) in combination, the doseresponse curve for the effect of instilled BK (PD100 = 1.1 nmol, 95% c.i. 0.37-3.2 nmol) was similar to that obtained in the presence of each inhibitor used alone. 5The kininase I inhibitor, DL-2-mercaptomethyl-3-guanidinoethylthiopropionic acid (50 nmol instillation) failed to alter the dose-response curve to instilled BK (PD1oo = 14.6nmol, 95% c.i. 6.7-32.0 nmol). 6 These data suggest that both ACE and NEP degrade BK in the airway lumen, but that kininase I is not involved.

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Section: Discussionmentioning

confidence: 99%

The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

Ichinose¹,

Barnes²

1990

British J Pharmacology

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“…Cough is a well documented side effect of ACE inhibitors and an expected adverse event for moexipril in the whole population. [34][35][36][37] Although the ability is limited to extrapolate the findings to other HRT groups than those examined, this study indicates that moexipril is effective and well-tolerated in the treatment of hypertensive, postmenopausal women and can safely be co-administered to individuals taking HRT. Nevertheless, the interaction of ACE inhibition and HRT during longterm administration in postmenopausal women remains an outstanding topic which requires further research.…”

Section: Discussionmentioning

confidence: 83%

Co-administration of an ACE-inhibitor (moexipril) and hormonal replacement therapy in postmenopausal women

1999

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Co-administration of antihypertensive drug therapy and hormonal replacement therapy (HRT) is frequent in postmenopausal women but it is not known whether HRT interacts with concomitant antihypertensive therapy. The present study was designed to investigate efficacy and safety of the ACE inhibitor moexipril in comparison to placebo in hypertensive, postmenopausal women on HRT.After a 4-week placebo run-in phase, 95 postmenopausal women (35-74 years of age) who had a sitting diastolic blood pressure (BP) of 95-114 mm Hg and were treated with HRT were randomised to a 12-week treatment with moexipril 15 mg or placebo. Efficacy and safety were assessed by measuring changes in sitting BP and metabolic parameters associated with cardiovascular disease including triglycerides, total cholesterol, HDL, LDL, total cholesterol/HDL ratio and glucose. Adverse events were recorded continuously.After 12 weeks of treatment, moexipril 15 mg was significantly more effective in reducing sitting systolic

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“…ACE inhibitor cough is probably mediated by C-fibres in the upper respiratory tract, as patients with this side-effect have increased sensitivity of the cough reflex to inhaled capsaicin, which acts specifically on C-fibres [13]. Patients with ACE inhibitor cough thus show a shift to the left of the dose-response to inhaled capsaicin [13,14].…”

Section: Introductionmentioning

confidence: 99%

8 Effect of dose adjustment on enalapril-induced cough and the response to inhaled capsaicin

Yeo

Higgins

Foster

et al. 1994

Journal of Hypertension

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1 In nine hypertensive patients with enalapril-induced cough the effect of altering the dose of enalapril on subjective cough and the cough response to inhaled capsaicin was examined in a random single-blind balanced cross-over study. They received three doses of enalapril, each for 3 weeks; the dose at entry (mean 10 mg daily); double this dose (mean 20 mg daily); and half this dose (mean 5 mg daily). 2 The cough response to inhaled capsaicin was also measured in two control groups:hypertensive patients on long-term enalapril treatment with no cough (n = 18), and hypertensive patients taking nifedipine (n = 17). 3 In patients with enalapril-induced cough there were significant dose-responses for enalapril as regards severity of cough (P < 0.05) and night time waking by cough (P < 0.05), but not for frequency of cough. Although the cough was less severe (P < 0.02) and caused less night time waking (P < 0.03) on the lowest dose of enalapril (mean 5 mg daily) it did not disappear completely in any patient. 4 The sensitivity to inhaled capsaicin did not differ significantly on the three doses of enalapril. The relative potency of capsaicin on enalapril 20 mg compared with enalapril 5 mg was 1.0 (95% CI 0.4-2.2). The wide confidence limits indicate that an important dose-dependent shift in capsaicin sensitivity is not excluded. 5 The sensitivity to inhaled capsaicin differed significantly between patients with enalapril-induced cough and both control groups. The relative potency of capsaicin was 0.2 (95% CI 0.1-0.4, P < 0.001) in patients taking nifedipine, and 0.4 (95% CI 0.2-0.8, P < 0.005) in patients taking enalapril who had no cough, when compared with patients with enalapril-induced cough. 6 The dose-response for capsaicin was shifted significantly to the left in patients on enalapril who had no cough when compared with patients taking nifedipine (relative potency 0.5, 95% CI 0.3-1.0, P < 0.05). 7 In patients with enalapril-induced cough reducing the dose improves the severity of cough and night time waking, but this may be of limited value as the cough persisted to some degree in all patients. 8 The enhanced sensitivity to capsaicin in patients taking enalapril who had no cough suggests that ACE inhibitors may alter the cough reflex in all patients, with those who develop cough representing the extreme of this general shift. This hypothesis needs to be tested in a larger prospective study.

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Increased cough reflex associated with angiotensin converting enzyme inhibitor cough.

Cited by 114 publications

References 4 publications

The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

Co-administration of an ACE-inhibitor (moexipril) and hormonal replacement therapy in postmenopausal women

8 Effect of dose adjustment on enalapril-induced cough and the response to inhaled capsaicin

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