Kir6.1-dependent K_ATP channels in lymphatic smooth muscle and vessel dysfunction in mice with Kir6.1 gain-of-function.

ABSTRACT:

Key points

Spontaneous contractions are essential for normal lymph transport and these contractions are exquisitely sensitive to the K_ATP channel activator pinacidil. K_ATP channel Kir6.1 and SUR2B subunits are expressed in mouse lymphatic smooth muscle (LSM) and form functional K_ATP channels as verified by electrophysiological techniques. Global deletion of Kir6.1 or SUR2 subunits results in severely impaired lymphatic contractile responses to pinacidil. Smooth muscle-specific expression of Kir6.1 gain-of-function mutant (GoF) subunits results in profound lymphatic contractile dysfunction and LSM hyperpolarization that is partially rescued by the K_ATP inhibitor glibenclamide. In contrast, lymphatic endothelial-specific expression of Kir6.

SUBMITTER: Davis MJ 

PROVIDER: S-EPMC7641979 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature