Englerin A (EA) is a potent agonist of tetrameric transient receptor potential canonical (TRPC) ion channels containing TRPC4 and TRPC5 subunits. TRPC proteins form cation channels that are activated by plasma membrane receptors. They convert extracellular signals such as angiotensin II into cellular responses, whereupon Na and Ca influx and depolarization of the plasma membrane occur. Via depolarization, voltage-gated Ca (CaV) channels can be activated, further increasing Ca influx. We investigated the extent to which EA also affects the functions of CaV channels using the high-voltage-activated L-type Ca channel CaV1.2 and the low-voltage-activated T-type Ca channels CaV3.1, CaV3.2 and CaV3.3. After expression of cDNAs in HEK293 cells, EA inhibited currents through all T-type channels at half-maximal inhibitory concentrations (IC ) of 7.5 to 10.3 µM. In zona glomerulosa cells of the adrenal gland, angiotensin II-induced elevation of cytoplasmic Ca concentration leads to aldosterone release. We identified transcripts of low- and high-voltage-activated CaV channels and of TRPC1 and TRPC5 in the human zona glomerulosa cell line HAC15. While no EA-induced TRPC activity was measurable, Ca channel blockers distinguished T- and L-type Ca currents. EA blocked 60% of the CaV current in HAC15 cells and T- and L-type channels analyzed at -30 mV and 10 mV were inhibited with IC values of 2.3 and 2.6 µM, respectively. While the T-type blocker Z944 reduced basal and angiotensin II-induced 24-hour aldosterone release, EA was not effective. In summary, we show here that EA blocks CaV1.2 and T-type CaV channels at low-micromolar concentrations. In this study we showed that englerin A (EA), a potent agonist of TRPC4- or TRPC5-containing tetrameric TRPC channels and currently under investigation to treat certain types of cancer, also inhibits L-type voltage-gated CaV1.2 and T-type voltage-gated CaV3.1, CaV3.2 and CaV3.3 Ca channels at low-micromolar concentrations.