| Summary: | 碩士 === 國立臺灣大學 === 藥理學研究所 === 81 === YC-1 inhibited the aggregation and ATP release of washed rabbit
platelets induced by U46619, arachidonic acid, collagen,PAF and
thrombin.YC-1 markedly activated guanylate cyclase in platelet
homogenate and soluble fraction, and markedly elevated cGMP and
cAMP levels in intact platelets. These results suggest that the
increase in platelet cAMP caused by YC-1 is mediated by the in-
hibition by cGMP of cAMP breakdown, and the antiplatelet effect
of YC-1 is likely due to the elevation of both cGMP and cAMP
levels. CES-L and Pro-A2 inhibited the rabbit platelet aggrega-
tion and ATP release induced by arachidonic acid (AA) and coll-
agen, without affecting those induced by U46619,PAF and throm-
bin. Thromboxane B2 and prostaglandin D2 formation caused by AA
were also suppressed by both antiplatelet agents.CES-L and Pro-
A2 inhibited the rise of intracellular calcium concentration
caused by AA and collagen, and also suppressed the generation
of inositol monophosphate caused by AA,but not that by
collagen, U46619, PAF and thrombin.These results suggest that
the antipla- telet effect of both CES-L and Pro-A2 is likely
due to the inhi- bition of thromboxane A2 formation.
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