Background. How the kidney regulates iodide excretion is poorly understood. Iodide elimination occurs primarily through the kidney, being excreted in urine as inorganic iodide. Iodide is freely filtered at the glomerulus and partially reabsorbed along the tubular epithelium through both passive and active mechanisms. However, the events involved in its tubular recovery are poorly characterized.
Originally identified in the thyroid, the Na+/I- symporter (NIS) is an integral plasma membrane glycoprotein able to specifically mediate iodide transport in many tissues, playing an important role in iodide metabolism. Interestingly, NIS expression was demonstrated in the renal tubular system, suggesting that NIS might be involved in renal iodide transport.
Objective. To investigate a role of NIS-mediated iodide reabsorption, we examined the regulation of renal NIS expression by high plasma iodide concentrations.
Methods. Male Wistar rats were subjected to iodide rich diet (0.05% I--supplemented drinking water) for 1, 2 and 6 days in the chronic experiments (n=8/group), or received a single 0.01, 0.1 or 1 mg ip injection of iodide for 24 h in the acute model (n=4/group). Thereafter, total kidney RNA extraction was performed and NIS mRNA abundance was evaluated by real-time PCR.
Results. We observed a significant reduction of NIS mRNA abundance in rats subjected to chronic iodide ingestion after 2 and 6 days. Similarly, in the acute model, we measured a significant decrease of NIS mRNA expression at all the tested concentrations of iodide.
Conclusions. High plasma iodide concentrations repressed renal NIS mRNA expression. Thus, these findings lead to propose a potential role of NIS in the renal regulation of iodide excretion; in turn contributing to the maintenance of iodide homeostasis.
