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YC-1, a novel activator of platelet guanylate cyclase
FN Ko, CC Wu, SC Kuo, FY Lee and CM Teng
Pharmacological Institute, College of Medicine, National Taiwan University,
Taipei.
YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole] inhibited the
aggregation of and ATP release from washed rabbit platelets induced by
arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF),
and thrombin in a concentration-dependent manner. YC-1 also disaggregated
the clumped platelets caused by these inducers. The thromboxane B2
formation caused by collagen, PAF, and thrombin was inhibited by
concentrations of YC-1 that did not affect formation of thromboxane B2 and
prostaglandin D2 caused by AA. YC-1 suppressed the increase of
intracellular Ca2+ concentration and generation of inositol
1,4,5-trisphosphate caused by these five aggregation inducers. Both the
cAMP and cGMP contents of platelets were increased by YC-1 in a
concentration- and time-dependent manner. Like sodium nitroprusside, YC- 1
potentiated formation of cAMP caused by prostaglandin E1 but not that by
3-isobutyl-1-methylxanthine. Adenylate cyclase and cAMP phosphodiesterase
activities were not altered by YC-1. Activity of cGMP phosphodiesterase was
unaffected by YC-1. Activities of guanylate cyclase in platelet homogenate
and cytosolic fraction were activated by YC-1, whereas particulate
guanylate cyclase activity was unaffected. The antiplatelet effect of
sodium nitroprusside but not that of YC-1 was blocked by hemoglobin and
potentiated by superoxide dismutase. After intraperitoneal administration
for 30 minutes, YC-1 prolonged the tail bleeding time of conscious mice.
These data indicate that YC-1 is a direct soluble guanylate cyclase
activator in rabbit platelets. It may also possess antithrombotic potential
in vivo.
Volume 84,
Issue 12,
pp. 4226-4233,
12/15/1994
Copyright © 1994 by The American Society of Hematology
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