1. Using front-surface fluorometry of fura-2-loaded strips, and measuring the transmembrane 45Ca2+ fluxes of ring preparations of the rabbit femoral artery, the mechanism underlying a sustained decrease in the cytosolic Ca2+ concentration ([Ca2+](i)) induced by angiotensin II (AT-II) was investigated. 2. The application of AT-II during steady-state 118 mM K+-induced contractions caused a sustained decrease in [Ca2+](i) following a rapid and transient increase in [Ca2+](i), while the tension was transiently enhanced. 3. When the intracellular Ca2+ stores were depleted by thapsigargin, the initial rapid and transient increase in [Ca2+](i) was abolished, however, neither the sustained decrease in [Ca2+](i) nor the enhancement of tension were affected. 4 Depolarization with 118 mM K+ physiological salt solution containing 1.25 mM Ba2+ induced a sustained increase in both the cytosolic Ba2+ concentration ([Ba2+](i)) level and tension. However, the application of 10-6 M AT-II during sustained Ba2+-contractions was found to have no effect on [Ba2+](i), but it did enhance tension. 5. After thapsigargin treatment, AT-II neither decreased nor increased the enhanced Ca2+ efflux rate induced by 118 mM K+-depolarization, whereas AT-II did increase the enhanced 45Ca2+ influx and the 45Ca2+ net uptake induced by 118 mM K+-depolarization. 6. Pretreatment with calphostin-C, partially, but significantly inhibited the decrease in [Ca2+](i) induced by AT-II. 7. These findings therefore suggest that AT-II stimulates Ca2+ sequestration into the thapsigargin insensitive Ca2+ stores, and thus induces a decrease in [Ca2+](i) in the high external K+-stimulated rabbit femoral artery.
- Vascular smooth muscle
ASJC Scopus subject areas