M. Vanwyk et al., EFFECTS OF GLYCOPYRROLATE ON CAPSAICIN-INDUCED COUGH IN NORMAL VOLUNTEERS TREATED WITH CAPTOPRIL, European Journal of Clinical Pharmacology, 46(5), 1994, pp. 437-439
The effects of inhibition of angiotensin converting enzyme (ACE) and g
lycopyrrolate on cough caused by inhaled capsaicin were investigated i
n a double-blind, randomised cross-over study in twelve normal volunte
ers. The capsaicin challenge was performed before and 2 h after dosing
with 75 mg captopril or matched placebo given orally, and 20, 40 and
60 min after giving 1 mg glycopyrrolate IV to each subject. Captopril
and placebo did not alter the cough response when compared to baseline
. Glycopyrrolate, however, caused a significant increase in the thresh
old sensitivity (D-2) from baseline, and a significant decrease in the
total cough response at 40 and 60 min both after captopril and placeb
o. The D-2-baseline and D-2-40 min after glycopyrrolate (mean (SD), re
spectively, were 3.2 (1.0); 17.9 (4.2) after placebo and 2.5 (8.5); 23
.6 (6.9) after captopril. Elimination of vagal influences implies atte
nuation of the effects of tachykinins but not those prostaglandins. We
postulate that tachykinins, such as substance P, play a more importan
t role than prostaglandins in capsaicin-induced cough. We conclude tha
t the vagus is important in the capsaicin-induced cough reflex, but, a
s suppression of this reflex by glycopyrrolate was delayed, the releva
nt receptors are either poorly accessible peripheral receptors or they
are located in the central nervous system.