Effects of nifedipine on nerve-evoked action potentials and consequent contractions in rat tail artery

Abstract

The effects of nifedipine on the electrical and mechanical activity recorded from the rat tail artery were examined. Intracellular recordings were obtained from the smooth muscle and vessel diameter monitored during nerve stimulation. Nifedipine (0.1–10 μM) depressed contractions elicited by single and repetitive (2 Hz) stimulation by 32–100% but was ineffective in decreasing the amplitude of the associated action potentials. Concentrations ≥10 μM caused a slowly developing membrane depolarization. No change in the amplitude of subthreshold excitatory junction potentials was observed at concentrations of nifedipine less than 50 μM when the membrane depolarization was less than 8 mV. At all concentrations examined nifedipine lowered the stimulus intensity required to initiate an action potential. The amplitude of the nerve-evoked action potential recorded in lowered external Ca²⁺ (1 mM) was slightly increased (5–10%) by nifedipine. However, nifedipine readily reversed the increased amplitudes of the nerve-evoked action potentials and contractions caused by the addition of 20 mM tetraethylammonium chloride in the tail artery. The action potential recorded in normal solution from the guinea pig vas deferens was selectively abolished by nifedipine.