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Vol. 283, Issue 2, 548-556, 1997
Division of Molecular Cardiology, Research Institute of
Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka
812-82, Japan
By use of front-surface fluorometry and fura-2-loaded medial strips of
the porcine coronary artery, cytosolic Ca++ concentration
([Ca++]i) and force development were
monitored simultaneously to determine the mechanisms of vasorelaxation
induced by the diadenosine polyphosphates (APnA)
diadenosine 5
,5
-P1,P4-tetraphosphate
(AP4A) and diadenosine
5,5-P1,P5-pentaphosphate
(AP5A). APnA concentration-dependently
inhibited the sustained elevations of [Ca++]i
and force induced by U-46619, a thromboxane A2 analog, in
the presence of extracellular Ca++. APnA
shifted the [Ca++]i-force relation curves of
contractions induced by various concentrations of high K+
to the right. The AP4A-induced decreases in
[Ca++]i and force were largely attenuated by
tetrabutylammonium. The AP4A-induced decreases in force
were attenuated by 4-aminopyridine and charybdotoxin. The
AP5A-induced decreases in [Ca++]i
and force were attenuated by tetrabutylammonium, 4-aminopyridine and
charybdotoxin. In the absence of extracellular Ca++,
APnA did not inhibit the transient elevations of
[Ca++]i induced by histamine or caffeine.
Both AP4A and AP5A increased intracellular cAMP
content. We thus conclude that AP4A and AP5A relax the porcine coronary artery by decreasing
[Ca++]i, possibly through the activation of
K+ channels, but not through inhibition of intracellular
Ca++ release and by decreasing the Ca++
sensitivity of the contractile machinery. These effects were considered
to be mediated by cAMP.
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