The mechanism of the decrease in cytosolic Ca2+ concentrations induced by angiotensin II in the high K+-depolarized rabbit femoral artery

Masuko Fukai, Hiromichi Yamamoto, Junji Nishimura, Katsuya Hirano, Hideo Kanaide

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)437-447
Number of pages11
JournalBritish Journal of Pharmacology
Volume129
Issue number3
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

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Femoral Artery
Angiotensin II
Rabbits
Thapsigargin
Fluorometry
Fura-2
Salts

Keywords

  • Angiotensin-II
  • Calcium
  • Vascular smooth muscle

ASJC Scopus subject areas

  • Pharmacology

Cite this

The mechanism of the decrease in cytosolic Ca2+ concentrations induced by angiotensin II in the high K+-depolarized rabbit femoral artery. / Fukai, Masuko; Yamamoto, Hiromichi; Nishimura, Junji; Hirano, Katsuya; Kanaide, Hideo.

In: British Journal of Pharmacology, Vol. 129, No. 3, 01.01.2000, p. 437-447.

Research output: Contribution to journalArticle

Fukai, Masuko ; Yamamoto, Hiromichi ; Nishimura, Junji ; Hirano, Katsuya ; Kanaide, Hideo. / The mechanism of the decrease in cytosolic Ca2+ concentrations induced by angiotensin II in the high K+-depolarized rabbit femoral artery. In: British Journal of Pharmacology. 2000 ; Vol. 129, No. 3. pp. 437-447.
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N2 - 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.

AB - 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.

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