Calcium channel blockers promote vasodilator activity (and reduce blood pressure) by reducing calcium influx into vascular smooth muscle cells.

Anesthesia and calcium channel blocker: Calcium channel blockers can have significant interactions with anesthetic agents.

All agents appear to potentiate both depolarizing and nondepolarizing neuromuscular blocking agents and the circulatory effects of volatile agents.
Verapamil may also modestly decrease anesthetic requirements. Both verapamil and diltiazem can potentiate depression of cardiac contractility and conduction in the AV node by volatile anesthetics.
Nifedipine potent effects on the systemic blood pressure may precipitate hypotension, reflex tachycardia, or both; its fast-onset preparations (eg, sublingual) have been associated with MI in some patients.
Calcium channel blockers potentiate the hypotensive effects of volatile anaesthetics Verapamil (and to a lesser extent diltiazem) has additive effects with halothane on cardiac conduction and contractility, with the potential for bradycardia and myocardial depression.
Plasma concentrations of verapamil are increased during anaesthesia with volatile agents, possibly because of decreased hepatic blood flow.
Verapamil has been shown to decrease the MAC of halothane; nifedipine enhances the analgesic effects of morphine.