Recently we found that the sodium-bicarbonate co-transporter, NBCn1, is expressed in both endothelial cells and vascular smooth muscle cells where it regulates intracellular pH and through this modifies vascular tone. The pathways involved in regulation of NBCn1 are largely unknown. To address this we aimed at determining the genetic environment for NBCn1. A bioinformatic search was performed. Based on alignments of the gene primary structure in different species, it was revealed that in all known mammals the NBCn1 gene was followed by a serine/threonine kinase, NEK10. This association was also found in the G. gallus and O. anatinus genome, while in C. elegans the NBCn1 was associated with a closely related kinase. We produced a NBCn1 KO mouse containing a disruption of the promoting region of NBC1 and found surprisingly that in these mice also lacked NEK10 expression, while in heterozygous mice both genes had reduced expression compared to WT mice. This could indicate a dicistronic transcription. To test this possibility, RT-PCR was performed with a forward primer in NBCn1 and a reverse primer in NEK10. Sequencing of the product revealed the presence of mRNA containing both NBCn1 and NEK10 with an intermediary unknown segment. To test possible co- regulation of the two genes, the expression was evaluated in kidneys from potassium-depleted mice. In potassium-depleted mice, NBCn1 was markedly up regulated in the outer medulla of mice kidney at day 4 and 7 and this was also the case for NEK10. The present findings suggest that dicistronic transcription – which is rare in the mammalian genome - of NBCn1 and NEK10 occurs. The data also indicate that the two genes are co-regulated possible consequent to being under control of the same promoter. It remains to be investigated whether NEK10 expression is functionally important for NBCn1 activity and hence potentially for vascular function.