Previous observations have documented increased pressure-induced (myogenic) tone in small uteroplacental arteries from late pregnant (LP) rats. In this study, we hypothesized that this response may result from a diminished activity of vascular smooth muscle cell (SMC) K_v channels, leading to membrane depolarization, augmented Ca²⁺ influx, and vasoconstriction (tone). Elevation of intraluminal pressure from 10 to 60 and 100 mm Hg resulted in a marked, diltiazem-sensitive rise in SMC [Ca²⁺]_i associated with a vasoconstriction of uteroplacental arteries of LP rats. In contrast, these changes were significantly diminished in uterine arteries from NP rats. Gestational augmentation of pressure-induced Ca²⁺ influx through L-type Ca²⁺ channels was associated with an enhanced SMC depolarization, the appearance of electrical and Ca²⁺ oscillatory activity and vasomotion. Exposure of vessels from NP animals to 4-AP, which inhibits the activity of K_v channels, mimicked the effects of pregnancy by increasing pressure-induced depolarization, elevation of [Ca²⁺]_i , and development of myogenic tone. Furthermore, currents through K_v channels were significantly reduced in myocytes dissociated from arteries of LP rats compared to those of NP controls. Based on these results, we conclude that decreased K_v channel activity importantly contributes to enhanced pressure-induced depolarization, calcium entry and the increase in myogenic tone present in uteroplacental arteries from late pregnant rats.