Journal of Applied Physiology, Vol 55, Issue 5 1496-1500, Copyright © 1983 by American Physiological Society
Importance of calcium in citric acid-induced airway constriction
H. Downes and C. A. Hirshman
In previous studies, a 5-min inhalational challenge with 10% citric acid
aerosol (0.52 M) elicited bronchoconstriction in Basenji-Greyhound (BG)
dogs with hyperreactive airways but not in mongrel dogs. This response was
independent of vagal reflexes because it was not attenuated by atropine.
Citric acid might elicit bronchoconstriction because of acidity, calcium
chelation, or some other effect of the citrate molecule. To assess these
factors, barbiturate-anesthetized BG dogs were challenged (5 min) with
aerosols of 10% acetic acid or a citric acid (0.48 M)/Na3citrate (0.04 M)
mixture of equivalent pH, 6% Na2-ethylenediaminetetraacetic acid (EDTA), or
6% CaNa2EDTA. Each challenge was delivered in a separate week. The acidity
alone was not an adequate stimulus, since pulmonary resistance (RL) was
unaltered by 10% acetic acid, although markedly increased by the citric
acid-Na3citrate mixture [2.2 +/- 0.4 (SE) cmH2O X l-1 X s prechallenge,
10.0 +/- 2.2 postchallenge]. Aerosols of Na2EDTA provoked a similar
increase in RL (2.1 +/- 0.4 cmH2O X l-1 X s prechallenge, 9.0 +/- 1.8
postchallenge). Neither effect was attenuated by intravenous atropine (0.2
mg/kg). CaNa2EDTA caused no changes in RL. We conclude that it is the
calcium chelating action of citric acid rather than its acidity that is
responsible for bronchoconstriction in BG dogs with hyperreactive airways.
