Calcium, the control of smooth muscle function and bronchial hyperreactivity

Area of Science:

• Physiology
• Pharmacology

Background:

• Smooth muscle excitation-contraction coupling relies on intracellular and extracellular calcium sources.
• Extracellular calcium enters smooth muscle through receptor-operated (ROC) and potential-dependent (PDC) channels.
• PDC channels are sensitive to calcium channel antagonists like verapamil, nifedipine, and diltiazem.

Purpose of the Study:

• To review calcium mobilization in respiratory smooth muscle.
• To investigate the role of extracellular calcium in tracheal smooth muscle responses to various stimulants.
• To explore the potential link between calcium channel function and bronchial hyperreactivity.

Main Methods:

• Review of existing evidence on calcium mobilization in respiratory smooth muscle.
• Studies on bovine, canine, and guinea pig tracheal muscle.
• Analysis of calcium-dependence of muscle response and sensitivity to calcium channel antagonists.

Main Results:

• Both intracellular and extracellular calcium sources are utilized in respiratory smooth muscle.
• The order of extracellular calcium utilization by tracheal smooth muscle was K+ > histamine ≥ 5-hydroxytryptamine > acetylcholine.
• Calcium channel antagonists exhibit bronchodilator activity.

Conclusions:

• A defect in calcium mobilization or receptor-calcium coupling may underlie bronchial hyperreactivity.
• Calcium channel antagonists show potential therapeutic value for bronchial hyperreactivity.
• Similarities exist between respiratory smooth muscle reactivity and hypertensive vascular smooth muscle.