The contractile response of vascular smooth muscle to mechanical stretch, first observed in isolated segments of canine carotid artery by Bayliss [1], is often postulated to be a mechanism of myogenic control of blood flow. In most cell types, a transient increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) has been observed when cells are exposed to mechanical stress, and this increase is considered to be attributable to Ca 2ϩ influx through mechanosensitive ion channels [2]. Furthermore, the contraction in response to mechanical stimulation such as stretch has been known to be rate-dependent in the rat portal vein [3], the rabbit basilar artery [4], and the hamster cheek pouch arterioles [5]. Our previous studies indicated that the basilar arteries isolated from rabbit [4] and dog [6] treated with potassium channel blocker such as tetraethylammonium (TEA) easily produced contraction in response to a mechanical stimulation with varying rates of stretch. However, little information is available about the mechanotransduction mechanism, i.e., the signal transduction pathway that mediates conversion of mechanical stress to the specific cellular response including [Ca 2ϩ ] i mobilization and contraction. The cellular mechanisms underlying the effect of potassium blockers on the mechanotransduction also still remain unclear. Japanese Journal of Physiology, 51, 327-335, 2001 Key words: smooth muscle, basilar artery, mechanical stimulation, contraction, calcium.Abstract: Stretch evoked a contraction in a rate-dependent manner in canine basilar artery; slow stretch at rates less than 3 mm/s produced no active tension, whereas quick stretch at rates over 5 mm/s did. Large conductance Ca 2ϩ -activated K ϩ channel blockers, including charybdotoxin, iberiotoxin, and tetraethylammonium (TEA) sensitized the basilar artery to mechanical stimulation. TEA shifted the stretch rate-tension relationship toward the left. Thus, in the presence of TEA, the slow stretch (0.1-3 mm/s) could increase in intracellular Ca -insensitive component of quick stretch-induced contraction was eliminated by thapsigargin, but not by nicardipine. Ryanodine, cyclopiazonic acid, thapsigargin, U-73122, and calphostin C also abolished the nicardipineinsensitive component of quick stretch-induced contraction. These results suggest that the slow stretch-induced contraction was exclusively dependent on the Ca 2ϩ influx through L-type voltage-dependent Ca 2ϩ channels (VDCs), whereas the quick stretch-induced contraction was dependent on Ca 2ϩ release from sarcoplasmic reticulum (SR) and Ca 2ϩ influx through L-type VDCs.