Bradykinin Stimulates Renal Na⁺ and K⁺ Excretion by Inhibiting the K⁺ Channel (Kir4.1) in the Distal Convoluted Tubule.

ABSTRACT: Stimulation of BK2R (bradykinin [BK] B2 receptor) has been shown to increase renal Na⁺ excretion. The aim of the present study is to explore the role of BK2R in regulating Kir4.1 and NCC (NaCl cotransporter) in the distal convoluted tubule (DCT). Immunohistochemical studies demonstrated that BK2R was highly expressed in both apical and lateral membrane of Kir4.1-positive tubules, such as DCT. Patch-clamp experiments demonstrated that BK inhibited the basolateral 40-pS K⁺ channel (a Kir4.1/5.1 heterotetramer) in the DCT, and this effect was blocked by BK2R antagonist but not by BK1R (BK B1 receptor) antagonist. Whole-cell recordings also demonstrated that BK decreased the basolateral K⁺ conductance of the DCT and depolarized the membrane. Renal clearance exp

SUBMITTER: Zhang DD 

PROVIDER: S-EPMC6043363 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature