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Aim: To evaluate the influence of the vascular endothelial growth factor A (VEGFA) polymorphisms on risk of presentation with intracerebral hemorrhage (ICH)., Methods: Nine selected VEGFA single-nucleotide polymorphisms (SNPs) were genotyped in 311 patients with brain arteriovenous malformations (BAVM) in a Chinese population. Associations between individual SNPs/haplotypes and the hemorrhage risk of BAVMs were evaluated using logistic regression analysis., Results: In the single-locus analysis, rs1547651 was associated with increased risk of ICH (adjusted OR=2.11, 95% CI=1.01-4.42 compared with the AA genotype). In particular, an increased risk for ICH was associated with this variant in female patients (adjusted OR=3.21, and 95% CI=0.99-10.36). Haplotype-based analyses revealed that haplotype 'GC' in block 1 and haplotype 'ACC' in block 2 were associated with a 30%-38% reduction in the risk of ICH in patients with BAVMs compared to the most common haplotype (P(sim)=0.033 and P(sim)=0.005, respectively). The protective effect of haplotype 'ACC' in block 2 was more evident in male patients and subjects with BAVMs of a size ≥3 cm (adjusted OR=0.57, 95% CI=0.34-0.97 and adjusted OR=0.57, 95% CI=0.31-0.86, respectively)., Conclusion: The results suggest that VEGFA gene variants may contribute to ICH risk of BAVM.

Aim: To investigate the effects of docosahexaenoic acid (DHA) on large-conductance Ca(2+)-activated K(+)(BK(Ca)) channels and voltage-dependent K(+) (K(V)) channels in rat coronary artery smooth muscle cells (CASMCs)., Methods: Rat CASMCs were isolated by an enzyme digestion method. BK(Ca) and K(V) currents in individual CASMCs were recorded by the patch-clamp technique in a whole-cell configuration at room temperature. Effects of DHA on BK(Ca) and K(V) channels were observed when it was applied at 10, 20, 30, 40, 50, 60, 70, and 80 micromol/L., Results: When DHA concentrations were greater than 10 micromol/L, BK(Ca) currents increased in a dose-dependent manner. At a testing potential of +80 mV, 6.1%+/-0.3%, 76.5%+/-3.8%, 120.6%+/-5.5%, 248.0%+/-12.3%, 348.7%+/-17.3%, 374.2%+/-18.7%, 432.2%+/-21.6%, and 443.1%+/-22.1% of BK(Ca) currents were increased at the above concentrations, respectively. The half-effective concentration (EC(50)) of DHA on BK(Ca) currents was 37.53+/-1.65 micromol/L. When DHA concentrations were greater than 20 micromol/L, K(V) currents were gradually blocked by increasing concentrations of DHA. At a testing potential of +50 mV, 0.40%+/-0.02%, 1.37%+/-0.06%, 11.80%+/-0.59%, 26.50%+/-1.75%, 56.50%+/-2.89%, 73.30%+/-3.66%, 79.70%+/-3.94%, and 78.1%+/-3.91% of K(V) currents were blocked at the different concentrations listed above, respectively. The EC(50) of DHA on K(V) currents was 44.20+/-0.63 micromol/L., Conclusion: DHA can activate BK(Ca) channels and block K(V) channels in rat CASMCs, and the EC(50) of DHA for BK(Ca) channels is lower than that for K(V) channels; these findings indicate that the vasorelaxation effects of DHA on vascular smooth muscle cells are mainly due to its activation of BK(Ca) channels.