Histamine-dependent prolongation by aldosterone of vasoconstriction in isolated small mesenteric arteries of the mouse

In arterioles, aldosterone counteracts the rapid dilatation (recovery) following depolarization-induced contraction. The hypothesis was tested that this effect of aldosterone depends on cyclooxygenase (COX)-derived products and/or nitric oxide (NO) synthase (NOS) inhibition. Recovery of the response to high K+ was observed in mesenteric arteries of wild-type and COX-2−/− mice but it was significantly diminished in preparations from endothelial NOS (eNOS)−/− mice. Aldosterone pretreatment inhibited recovery from wild-type and COX-2−/− mice. The NO donor sodium nitroprusside (SNP) restored recovery in arteries from eNOS−/− mice, and this was inhibited by aldosterone. Actinomycin-D abolished the effect of aldosterone, indicating a genomic effect. The effect was blocked by indomethacin and by the COX-1 inhibitor valeryl salicylate but not by NS-398 (10−6 mol/l) or the TP-receptor antagonist S18886 (10−7 mol/l). The effect of aldosterone on recovery in arteries from wild-type mice and the SNP-mediated dilatati...