Down syndrome fibroblasts are hyperresponsive to beta-adrenergic stimulation.

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Abstract
The hormonal response of human skin fibroblasts after exposure to .beta.-adrenergic agonists, prostaglandin(PG)E1 and cholera toxin was monitored by intracellular cAMP accumulation. Down''s syndrome (DS; trisomy 21) cells had an .apprx. 10-fold greater response to .beta.-adrenergic agonists than did either normal diploid skin fibroblasts or other aneusomic fibroblast strains (trisomy 13, 18 and 22). The altered response in DS fibroblasts was specific for .beta.-adrenergic agonists, because treatment of DS or control cells with PGE1 or cholera toxin resulted in the same degree of cAMP accumulation. Experiments with 3-isobutyl-1-methylxanthine, a cyclic nucleotide phosphodiesterase inhibitor, indicated increased response of DS fibroblasts was not primarily a function of altered cAMP degradation. Monosomy 21 cells responded less than normal diploid fibroblasts to stimulation by the .beta.-adrenergic agonist isoproterenol. Genetic information on chromosome 21 participates in regulating the .beta.-adrenergic response of human fibroblasts.