ABSTRACT
At tempts to demonstrate relaxat ion mediated by endothelium-derived hyperpolar iz ing factor ( E D H F ) i n resistance arteries o f the mouse have provided apparently confl ic t ing data. In the isolated aorta, carot id , coronary and mesenteric arteries f rom C 5 7 B L 6 mice, isometric tension recording revealed clear endothelium-dependent relaxat ion to acetylcholine i n each case. These relaxations were abolished i n a l l but the mesenteric artery by the presence o f an inh ib i tor o f N O synthase. In the mesenteric artery, the addi t iona l presence o f indomethacin was required to abol ish the relaxat ion. A n identical profile o f response was recorded i n arteries taken f rom ni tr ic oxide synthase knockou t mice (Chataigneau et al, 1999). In contrast, a l though relaxat ion in mesenteric arteries f rom the same strain o f w i l d type mice was b locked by ni t roL-arg in ine plus indomethacin, i n the knock out mice the relaxations were insensitive to this combina t ion but inhibi ted i n the presence o f raised extracellular potassium (30 m M ) . A similar profile was obtained wi th isolated femoral arteries f rom these mice ( W a l d r o n et al, 1999). These latter data suggested the presence o f relaxation mediated by E D H F i n the mesenteric and femoral arteries o f the N O synthase k n o c k out mice. The only major difference between the two studies was the fact that the mesenteric arteries studied i n the latter were bo th pressurized and perfused.
