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- VanWijk, MJ, et al.
(författare)
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Vascular function in preeclampsia
- 2000
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Ingår i: Cardiovascular research. - 0008-6363. ; 47:1, s. 38-48
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Tidskriftsartikel (refereegranskat)
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- Luksha, L, et al.
(författare)
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The mechanism of EDHF-mediated responses in subcutaneous small arteries from healthy pregnant women
- 2004
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Ingår i: American journal of physiology. Regulatory, integrative and comparative physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 286:6, s. R1102-R1109
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Tidskriftsartikel (refereegranskat)abstract
- We studied the importance of endothelium-derived hyperpolarizing factor (EDHF) vs. nitric oxide (NO) and prostacyclin (PGI2) in bradykinin (BK)-induced relaxation in isolated small subcutaneous arteries from normal pregnant women. We also explored the contribution of cytochrome P-450 (CYP450) product of arachidonic acid (AA) metabolism, hydrogen peroxide (H2O2), and gap junctions that have been suggested to be involved in EDHF-mediated responses. Isolated arteries obtained from subcutaneous fat biopsies of normal pregnant women ( n = 30) undergoing planned cesarean section were mounted in a wire-myography system. In norepinephrine-constricted vessels, incubation with NG-nitro-l-arginine methyl ester (l-NAME) resulted in a significant reduction in relaxation to BK. Simultaneous incubation with l-NAME and indomethacin failed to modify this response further. BK-mediated dilatation in the presence of K+-modified solution was decreased to similar level as obtained after incubation with l-NAME. Incubation with l-NAME abolished BK-induced responses in K+-modified solution. Sulfaphenazole, a specific inhibitor of CYP450 epoxygenase, and catalase (an enzyme that decomposes H2O2) did not affect the EDHF-mediated relaxation because concentration-response curves to BK were similar in arteries after incubation with l-NAME vs. l-NAME + sulfaphenazole and l-NAME + catalase. The inhibitor of gap junctions, 18α-glycyrrhetinic acid, significantly reduced BK-mediated relaxation both without and with incubation with l-NAME. We found that both NO and EDHF, but not PGI2, are involved in the endothelium-dependent dilatation to BK. BK-induced relaxation is almost equally mediated by NO and EDHF. CYP450 epoxygenase metabolites of AA or H2O2 do not account for EDHF-mediated response; however, gap junctions are involved in the EDHF-mediated responses to BK in subcutaneous small arteries in normal pregnancy.
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