Inositol uptake in rat aorta

3H-inositol uptake into deendothelialized aorta was linear for at least 2 h and was composed of both a saturable, Na+-dependent, and a nonsaturable, Na+-independent component. The Na+-dependent component of inositol uptake had a Km of 50 μM and a Vmax of 289 pmol/mg prot/h. Exposure to LiCl, ouabain, or Ca2+ - free Krebs-Ringer bicarbonate solution inhibited uptake. Metabolic poisoning with dinitrophenol, as well as incubation with phloretin, an inhibitor of carrier-mediated hexose transport, also inhibited uptake. Exposure to norepinephrine decreased inositol uptake, while phorbol myristate acetate was without effect. Isobutylmethylxanthine significantly increased inositol uptake, while the increased uptake due to dibutyryl cyclic AMP and forskolin were not statistically significant. Sodium nitroprusside, and activator of guanylate cyclase, and 8-bromo cyclic GMP, were without effect on uptake, as was methylene blue, an inhibitor of guanylate cyclase. Inositol uptake into the aorta was increased when the endothelium was allowed to remain intact, although this effect was likely due to uptake in both the endothelial and smooth muscle cells