Extreme hydrops fetalis and cardiovascular abnormalities in mice lacking afunctional Adrenomedullin gene

Adrenomedullin, a recently identified potent vasodilator, is expressed wide ly and has been suggested to have functions ranging from reproduction to br ood pressure regulation. To elucidate these functions and define more preci sely sites of Adm expression, we replaced the coding region of the Adm gene in mice with a sequence encoding enhanced green fluorescent protein while leaving the Adm promoter intact. We find that Adm(-/-) embryos die at midge station with extreme hydrops fetalis and cardiovascular abnormalities, incl uding overdeveloped ventricular trabeculae and underdeveloped arterial wall s. These data suggest that genetically determined absence of Adm may be one cause of nonimmune hydrops fetalis in humans.