Afferent renal nerves stimulate vasopressin (VP) secretion by activation of VPergic neurons of supraoptic (SON) and paraventricular nuclei (PVN). Therefore, intrarenal infusion of bradykinin (BK), which excites afferent renal nerves, increases VP release. However, BK is also a potent intrarenal vasodilatator hence BK may modulate VP secretion not only by stimulating its release via afferent renal nerves, but also inhibiting its renal effects as intrarenal vasodilator via a paracrine control. Furthermore, BK impaires the mechanism of phosphorilation that induces the traslocation of aquaporin 2 containing vesicles to the apical plasma membrane thus inhibiting the osmotic water permeability of the collecting duct cells induced by VP via its V2 receptor, a Gs protein-coupled receptor. In addition, BKB2 receptor knockout mice exhibit decreased urine volume and increased urine osmolality following water deprivation. Oxytocin (OT) increases urine output and sodium excretion in rats. Icatibant, a BKB2 antagonist, suppresses these effects showing that BK mediates diuresis and natriuresis induced by OT. Infusion of OT down-regulates myometrial OT and BK receptors indicating the existence of a common final pathway of OT and BK in the contractile responsiveness of uterine myometrial cells. The frequency of uterine contractions induced by OT and BK are stimulated by nitric oxide via prostaglandins release.