In pregnancy, α-adrenoceptor mediated vasoconstriction is augmented in uterine radial arteries, and is accompanied by underlying changes in smooth muscle (SM) Ca²⁺ activity. This study aims to determine the Ca²⁺ entry channels associated with altered vasoconstriction in pregnancy, with the hypothesis that augmented vasoconstriction involves transient receptor potential canonical type-3 (TRPC3) and L- and T-type voltage-dependent Ca²⁺ channels. Immunohistochemistry showed TRPC3, L-type Ca_v1.2 (as the α1C sub-unit), and T-type Ca_v3.1 (α1G) and Ca_v3.2 (α1H) localization to the uterine radial artery SM. Fluorescence intensity of TRPC3, Ca_v1.2 and Ca_v3.2 was increased, and Ca_v3.1 decreased in radial artery SM from pregnant rats. Western blotting confirmed increased TRPC3 protein expression in the radial artery from pregnant rats. Pressure myography incorporating pharmacological intervention to examine the role of these channels in uterine radial arteries showed an attenuation of phenylephrine (PE)-induced constriction with Pyr3-mediated TRPC3 inhibition, or with nifedipine-mediated L-type channel block alone in vessels from pregnant rats; both effects of which were diminished in radial arteries from non-pregnant rats. Combined TRPC3 and L-type inhibition attenuated PE-induced constriction in radial arteries; and the residual vasoconstriction was reduced, and abolished, with T-type channel block with NNC 55-0396 in arteries from non-pregnant and pregnant rats, respectively. With SM Ca²⁺ stores depleted, and in the presence of PE, nifedipine and NNC 55-0396, blockade of TRPC3 reversed PE-induced constriction. These data suggest that TRPC3 channels act synergistically with L-and T-type channels to modulate radial artery vasoconstriction, with the mechanism being augmented in pregnancy.