Dry air-induced bronchoconstriction--a role for voltage-sensitive calcium channels?

We examined the role played by voltage-sensitive calcium channels (VSCC) in airflow-induced bronchoconstriction (AIB). Collateral resistance (Rcs) in anesthetized male mongrel dogs was measured before and after periods of elevated airflow, or before and after hypocapnic challenge, using a wedged bronchoscope technique. A dihydropyridine calcium channel antagonist (nifedipine) was ineffective in preventing or even attenuating AIB in the canine lung periphery. Treatment with nifedipine did not affect the response of peripheral airways to aerosolized acetylcholine, indicating that receptor-operated calcium channels (ROCC) and/or release of calcium from intracellular stores were unaffected by this drug. Despite the ability of a calcium agonist (BAY K8644) to enhance responses to a hypocapnic challenge, it did not alter peripheral airway responses to dry air. Neither nifedipine nor BAY K8644 affected airway wall temperature at any time during the dry air experiments. We conclude that dihydropyridine receptors do not play a significant role in initiating AIB in the canine lung periphery.