Vanilloid receptors are activated by capsaicin, the pungent ingredient in hot pepper. They are also specifically and competitively inhibited by capsazepine (CPZ). To determine whether CPZ is specific to vanilloid receptors, its effects were tested on the currents evoked by nicotine in rat trigeminal ganglia. We found that 10 microM CPZ, a concentration frequently used to inhibit capsaicin's physiological responses attributed to capsaicin, reversibly inhibits (40%) the magnitude of the currents activated by 100 microM nicotine. We conclude that 10 microM capsazepine can alter the effects of channels other than those activated by capsaicin, and thus caution must be used in attributing all the CPZ-sensitive physiological effects to those only produced by blocking of vanilloid receptors.