Monoterpenes do not induce increases in [Ca2+]i in HEK cells expressing TRPV1 and TRPV4 channels. Representative traces demonstrating the unaltered [Ca2+]i baseline in HEK hTRPV1 (A) and HEK hTRPV4 (B) in the presence of 100 µM of carvacrol (#2), thymol (#3), β-myrcene (#4), α-terpinene (#5), and γ-terpinene (#6). Capsaicin (#1), the MTRPV1 agonist, and GSK-1016790A (#7), the TRPV4 agonist, were used to confirm the expressions of the TRPV1 and TRPV4 channels, respectively. Summarized data are shown in (C) and (D) for TRPV1 and TRPV4 HEK cells, respectively. The data are expressed as change in the [Ca2+]i influx from baseline to peak [Ca2+]i and plotted as mean ± SEM. * p < 0.0001 compared to agonist-induced [Ca2+]i influx. Statistical analysis was performed using one-way analysis of variance; n = 90 cells from 3 independent experiments.