The mechanism of action for the stimulatory effect of GH on longitudinal bone growth is not yet clarified. Several recent receptors indicate that GH has a direct effect at the site of the epiphyseal growth plate, as opposed to the somatomedin hypothesis which holds that the effect of GH is mediated by circulating insulin-like growth factors (IGFs). Using an RNA probe in a solution hybridization assay we investigated the presence of IGF-I mRNA in rat rib growth plate. Hypophysectomy resulted in a decrease in the number of IGF-I mRNA copies compared to that in normal rats. Replacement treatment with GH restored the number of transcripts in a specific and dose-dependent manner. The results show that GH regulates the level of IGF-I mRNA in rat rib growth plate and give further support to the hypothesis that locally produced IGF-I might contribute to the stimulatory effect of GH on longitudinal bone growth.