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Am J Physiol Regul Integr Comp Physiol (January 29, 2004). doi:10.1152/ajpregu.00550.2003
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Submitted on September 23, 2003
Accepted on January 28, 2004

The mechanism of EDHF-mediated responses in subcutaneous small arteries from healthy pregnant women

Leonid Luksha1, Henry Nisell1, and Karolina Kublickiene1*

1 Department of Obstetrics and Gynecology, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden

* To whom correspondence should be addressed. E-mail: Karolina.Kublickiene{at}klinvet.ki.se.

We studied the importance of EDHF versus 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 P450 (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 Nw-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, since concentration-response curves to BK were similar in arteries after incubation with L-NAME versus L-NAME+Sulfaphenazole and L-NAME+catalase. The inhibitor of gap junctions, 18{alpha}-GA, 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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