Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin.

Abstract Kinins, such as Bradykinin (BK), are peptide hormones of the kallikrein–kinin system. Apart from being a vasodilator, BK also increases urinary sodium excretion to reduce systemic blood pressure. It is becoming appreciated that BK modulates function of the epithelial Na + channel in the distal part of the renal nephron to affect tubular sodium reabsorption. In this chapter, we outline the molecular details, as well as discuss the physiological relevance of this regulation for the whole organism sodium homeostasis and setting chronic blood pressure.