SNP and was not modified at shorter times and lower SNP concentrations. An increase of cGMP was induced by TSH (Table 1). The inhibition exerted by SNP or 8-Br-cGMP for 24 h on the iodide uptake (131I) was reversed by

KT-5823 (1-10 mM), an inhibitor of thecGMP-dependent protein kinase (PKG) (Table 2). The TPO and TG mRNA expression (Northern-blot) was significantly reduced by 8-Br-cGMP. Data (24 h) were (Absorbance ratio mRNA/18 S rRNA, mean±SEM, arbitrary units): Control (C): TPO= 2.00, TG= 2.00; 8-Br-cGMP 100 mM: TPO= 1.97±0.24, TG= 1.96±0.03; 300 mM: TPO= 1.56±0.13, TG= 1.23±0.16**; 1000 mM: TPO= 1.22±0.29*, TG= 1.01±0.26** (*P<0.05, **P<0.01 vs C; n=3, ANOVA, Student-Newman-Keuls test). In conclusion, an activation of PKG seems to be involved in the NO/cGMP-induced inhibition of iodide uptake in FRTL-5. A reduction in the cAMP production could be relevant in the action of high NO/cGMP levels. Evidence is provided for a role of the cGMP pathway in the regulation of thyroid specific genes.