Cpa induces a sustained increase in [ca2+]i of endothelial cells in
situ and relaxes porcine coronary artery.
Higuchi, Yoshihiro, Junji Nishimura, Sei Kobayashi, Hideo Kanaide.
Division of Molecular Cardiology, Research Institute of
Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka 812,
Japan
APStracts 2:0514H, 1995.
Using fura-2 fluorometry, we investigated the effect of cyclopiazonic
acid (CPA), an inhibitor of Ca2+pump-ATPase of the endoplasmic
reticulum, on the cytosolic Ca2+ concentration ([Ca2+]i) and tension
in porcine aortic valvular endothelial cells and coronary arterial
strips with endothelium. In normal PSS, CPA induced a sustained
increase in [Ca2+]i of the valvular strips, while CPA elicited a
transient elevation of [Ca2+]i in Ca2+-free PSS. CPA (30 [mu]M)
relaxed coronary strips with endothelium precontracted by 100 nM
U46619, which was partially inhibited by Nw-nitro-L-arginine (L-NNA,
100 [mu]M). These results indicate that the CPA-induced increase in
[Ca2+]i depends both on the Ca2+ release and the Ca2+ influx in the
endothelial calls in situ, and that the CPA-induced endothelium
-dependent decreases in [Ca2+]i and tension in the smooth muscle is
due to the combined effect of L-NNA sensitive and resistant factors.
Received 17 October 1994; accepted in final form 3 November 1995.
APS Manuscript Number H927-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95