CPA induces a sustained increase in [Ca2+](i) of endothelial cells in situ and relaxes porcine coronary artery

Yoshihiro Higuchi, Junji Nishimura, Sei Kobayashi, Hideo Kanaide

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Abstract

Using fura 2 fluorometry, we investigated the effect of cyclopiazonic acid (CPA), an inhibitor of Ca2+ pump adenosinetriphosphatase of the endoplasmic reticulum, on cytosolic Ca2+ concentration ([Ca2+ ](i)) and tension in porcine aortic valvular endothelial cells and coronary arterial strips with endothelium. In normal physiological salt solution, CPA induced a sustained increase in [Ca2+](i) in the valvular strips, whereas in Ca2+- free physiological salt solution, CPA elicited a transient elevation of [Ca2+](i). CPA (30 μM) relaxed coronary strips with endothelium precontracted by 100 nM U-46619; this relaxation was partially inhibited by N(ω)-nitro-L-arginine (100 μM). These results indicate that the CPA- induced increase in [Ca2+](i) depends on the Ca2+ release and the Ca2+ influx in the endothelial cells in situ and that the CPA-induced endothelium- dependent decreases in [Ca2+](i) and tension in the smooth muscle are due to the combined effect of N(ω)-nitro-L-arginine-sensitive and -resistant factors.

Original languageEnglish
Pages (from-to)H2038-H2049
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume270
Issue number6 39-6
Publication statusPublished - Jun 1 1996

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All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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