Secretin (SCT), which was initially characterized as an intestinal hormone, has recently been found to play a role in fluid regulation. SCT and its receptor (SCTR) regulate the trafficking and expression of aquaporin 2 (AQP2) in renal principal cells independent of vasopressin (Vp). ANGII-induced water drinking and Vp release in central neurons depends also on the integrity of the SCT/SCTR axis (28). SCT can stimulate vasopressinergic and oxytocinergic neurons in the paraventricular nucleus (29), and it is hypothesized to be a neurohypophysial factor released into systemic circulation upon water deprivation or hyperosmolality. More recently, it was found that SCTR and ANGII receptor type 1 subtype a heteromer in central neurons mediates hyperosmolality-induced water intake in mouse. The functional interaction of receptors for SCT and ANGII thus raises the possibility that SCT may also participate in the regulation of sodium homeostasis in the periphery. In this report, we studied the function of SCT to regulate sodium retention via aldosterone under salt-restriction conditions.
