Thromboxane A2 (TXA₂) is a potent constrictor of fetoplacental arteries but little is known of the electromechanical events of smooth muscle contraction in these vessels. We reported previously that constriction of chorionic plate arteries (CPA’s) with U46619 (TXA₂ mimetic) is partially inhibited by nifedipine, a blocker of L-type voltage gated Ca²⁺ channels (VGCC’s) (Cooper et al. 2003). In this study we measured [Ca²⁺]_i and vessel diameter in pressurized CPA’s to test the hypothesis that TXA₂-induced constriction can by mediated by Ca²⁺ influx through nifedipine-sensitive and -insensitive pathways. CPA’s (199+17μm) were dissected from placentae at term following informed consent, loaded with the Ca²⁺ indicator dye Indo-1 (2 hours, 21°C) and mounted on an arteriograph at 25mmHg. Simultaneous recordings of intraluminal diameter and [Ca²⁺]_i (400:500nm fluorescence ratio at 360nm excitation) were made at 37°C. The effect of 10^-6M U46619 or 60mM KCl (high-K) (5 min) was examined in the presence and absence of extracellular Ca²⁺ with and without 10^-4M nifedipine. Statistical analyses were performed with Kruskal-Wallis and Dunns post hoc tests with p<0.05 taken as significant. High-K induced a maintained decrease in diameter of 10+4% and a concomitant increase in [Ca²⁺]_i (n=17;mean+SEM). Nifedipine significantly inhibited both responses by >95%. High-K had no effect on either vessel diameter or [Ca²⁺]_i in the absence of extracellular calcium. U46619 induced a 62+6% constriction (Fig.1B) and a peak increase in [Ca²⁺]_i followed by an elevated plateau, which were 51+11% and 50+10% of the high-K response respectively. Under Ca²⁺-free conditions, U46619 caused a small but significant peak increase in [Ca²⁺]_i probably due to Ca²⁺ release from intracellular stores. Re-addition of Ca²⁺ induced a large increase in [Ca²⁺]_i and a sustained constriction (Fig 1A,B). Nifedipine did not alter the responses to U46619 when extracellular Ca²⁺ was absent. When Ca²⁺ was re-introduced, nifedipine significantly reduced, but did not completely prevent, the rise in [Ca²⁺]_i and constriction (Fig 1A,B). We propose that constriction of human CPA’s in response to U46619 is mediated by nifedipine-sensitive VGCC’s and by nifedipine-insensitive Ca²⁺ entry.