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Calcium channel blockers modulate airway constriction in the canine lung periphery

K S Lindeman1, C A Hirshman, A N Freed

  • 1Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205.

Insights

Voltage-sensitive calcium channel blockers had varied effects on canine lung constriction. Verapamil partially reduced Na2EDTA-induced constriction, while nifedipine did not, suggesting limited calcium channel involvement in this specific response.

Area of Science:

  • Pulmonary Physiology
  • Pharmacology
  • Respiratory Medicine

Background:

  • Bronchoconstriction can be triggered by various stimuli, including chemical agents like disodium EDTA (Na2EDTA).
  • Voltage-sensitive calcium channels (VSCCs) play a role in smooth muscle contraction, including in the airways.

Purpose of the Study:

  • To investigate the role of VSCCs in Na2EDTA-induced bronchoconstriction in the canine lung periphery.
  • To compare the effects of nifedipine and verapamil on different bronchoconstrictive stimuli.

Main Methods:

  • Utilized a wedged bronchoscope technique in anesthetized dogs to measure collateral system resistance.
  • Administered aerosolized Na2EDTA, induced hypocapnia, aerosolized acetylcholine, and dry air challenges.
  • Assessed the impact of nifedipine (a dihydropyridine) and verapamil (a phenylalkylamine) on these induced responses.

Main Results:

  • Nifedipine significantly reduced hypocapnia-induced bronchoconstriction (88%) but had no effect on Na2EDTA-induced constriction.
  • Verapamil attenuated hypocapnia-induced (69%) and Na2EDTA-induced (44%) bronchoconstriction.
  • Neither blocker affected responses to acetylcholine or dry air challenges.

Conclusions:

  • Calcium influx via VSCCs plays a limited role in initiating Na2EDTA-induced bronchoconstriction in the canine lung periphery.
  • Different subtypes of VSCCs may be involved in mediating responses to various bronchoconstrictive stimuli.

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