We reported previously that the polymorphism frequency at R353Q of factor VII Japanese was not different from that of Caucasian and Afrocarribean populations, but was different from that of Gurjarati Indians (Scand J Clin Lab Invest 55: 211, 1995). There is another polymorphism that results in a 10 base pair insert in the promoter region at position -323 from the start of translation in the factor VII gene (0/10bp). Both polymorphisms were associated with lower levels of factor VII: c. However, it was reported that the polymorphism in the promoter region was not associated with lower levels of factor VII: c in Afrocarribeans (Thromb Haemost 77: 212, 1997). To examine the influence of genetic variability on race difference in factor VII, we examined the frequency of two polymorphisms of factor VII gene and the relationship between the polymorphisms and factor VII in 207 healthy Japanese individuals. The frequencies for the Q and 10bp allele were 0. 07 and 0. 08, respectively. The haplotype frequencies for R-0bp, R-10bp, Q-0bp and Q-10bp were 0. 909, 0. 021, 0. 011 and 0. 059, respectively. Factor VII: c, VII: ag and the binding ability to tissue factor (TF-VII binding) in individuals homozygous for 10bp were all approximately 30% lower than those without 10bp allele. Heterozygous 10bp individuals were approximately 12% higher than homozygous individuals. The frequency of homozygocity for both Q and 10bp was 1.45%, and their values related to factor VII were approximately 40% lower than those without 0bp and R allele. There was no difference in the levels of factor VII between smokers and non-smokers in spite of the presence and absence of polymorphisms in the factor VII gene. There was no difference in the correlation between factor VII and triglyceride in individuals with and without 10bp allele and/or Q allele.

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We investigated the effects of bradykinin (BK) on the regulatory mechanism of PGI₂ synthesis in endothelial cells with reference to intracellular Ca²⁺ kinetics, mRNA expression of cytosolic phospholipase A₂ (cPLA₂) and prostaglandin H₂ synthase-1 (PGHS-1).
PGI₂ generation increased with BK stimulation in a time dependent manner for 180 minutes. In the early phase of BK stimulation, intracellular Ca²⁺ ([Ca²⁺]i) concentration was increased by the influx of extracellular Ca2+ and a release from the Ca²⁺ storage site. However the increase of [Ca²⁺] i was observed for only 2 minutes.
cPLA₂ mRNA expression was 87 amol/μg RNA at rest. The additon of BK produced 746amol/μg RNA at 15 minutes. After pretreatment with cycloheximide, cPLA mRNA was superinduced. PGHS-1 mRNA expression was 562 amol/μg RNA at rest. The additon ofBK produced 10608 amol/μg RNA at 180 minutes. After pretreatment with cycloheximide, PGHS-1 mRNA expression was inhibited.
These results indicate that in the early phase of BK stimulation, [Ca²⁺]i activates cPLA₂, and cPLA₂ is considered to increase PGI₂ generation. After 2 minutes, the increase of cPLA₂ and PGHS-1 mRNA with BK stimulation seems to lead to an increase in these enzymes, but the time courses of these mRNA expressions were not the same.
It is suggested that BK induced PGI₂ generation depends not only on the increase of [Ca²⁺]i but also on the mRNA of cPLA₂ and PGHS-1.

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Acute myocardial infarction is known to be caused by thrombotic occlusion of coronary arteries. Although several investigators have suggested the abnormalities of plasma hemostatic parameters in patients with myocardial infarction, the relationship between these events and the onset of coronary thrombosis is still unclear. Recent in vitro investigations suggest the importance of the interaction between plasma ligand protein, von Willebrand factor (vWF), and platelet glycoproteins in the onset of arterial thrombosis, which occurs under the high shear stress of blood flow. In the present study, we investigated hemostatic abnormalities in patients with acute myocardial infarction by measuring plasma indicators including thrombin antithrombin III complex (TAT), plasminogen activator inhibitor 1 (PAI-1), the antigen level and ristocetin cofactor activities of vWF, and multimer analysis of vWF. In addition to hypercoagulabilities and increased antithrombolytic activities, a significant increase in antigen level or ristocetin cofactor activity of vWF was observed in patients with acute myocardial infarction. Although further study is needed, the increased levels of vWF in acute myocardial infarction may contribute to the re-occlusion of coronary artery after reperfusion treatment.

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