1. Two groups of eight normal subjects were investigated in separate studies to demonstrate the effects of changes in end-tidal Pco2, and of pretreatment with the calcium antagonist drug verapamil, on bronchoconstriction provoked by voluntary hyperventilation.
2. Total respiratory resistance (Ros) was measured by the forced oscillation technique before and after 90s voluntary hyperventilation. End-tidal Pco2 during hyperventilation was varied by altering inspired CO2 concentration. When end-tidal Pco2 fell during hyperventilation, there was a rise in Ros. This did not occur if end-tidal Pco2 was controlled at a normal resting level during hyperventilation.
3. Specific conductance (sGaw) was measured before and after 90 s voluntary hyperventilation of air. Subjects were treated with oral verapamil or placebo for 2 1/2 days and the effect of hyperventilation on sGaw was reassessed. Verapamil reduced significantly the fall in sGaw caused by hyperventilation. Placebo had no effect.
4. In normal humans, bronchoconstriction provoked by hyperventilating air at ambient temperature and humidity is mediated by the fall in Pco2, and is also reduced by verapamil.