Characterization of endothelium-derived hyperpolarizing factor in the human forearm microcirculation.

摘要: The identity of endothelium-dependent hyperpolarizing factor (EDHF) in the human circulation remains controversial. We investigated whether EDHF contributes to vasomotion forearm microvasculature by studying effect K+ and miconazole, an inhibitor cytochrome P-450, on response bradykinin healthy subjects. Study drugs were infused intra-arterially, blood flow was measured using strain-gauge plethysmography. Infusion KCl (0.33 mmol/min) into brachial artery caused baseline vasodilation inhibited vasodilator bradykinin, but not sodium nitroprusside. Thus incremental induced reduced from 14.3 +/- 2 7.1 ml x min(-1) 100 g(-1) (P < 0.001) after infusion. A similar inhibition = 0.014), nitroprusside (not significant), observed with study repeated during preconstriction phenylephrine restore resting basal values KCl. Miconazole (0.125 mg/min) did inhibit or -independent responses ACh nitroprusside, respectively. However, cyclooxygenase nitric oxide synthase aspirin NG-monomethyl-L-arginine, 0.003), significantly suppressed miconazole. oxide- prostaglandin-independent, bradykinin-mediated is high intravascular concentrations, indicating a contribution EDHF. In microvasculature, appears be P-450 derivative, possibly epoxyeicosatrienoic acid.