Genetic deficit of K_Ca 3.1 channels protects against pulmonary circulatory collapse induced by TRPV4 channel activation.

ABSTRACT:

Background and purpose

The intermediate conductance calcium/calmodulin-regulated K⁺ channel K_Ca 3.1 produces hyperpolarizing K⁺ currents that counteract depolarizing currents carried by transient receptor potential (TRP) channels, and provide the electrochemical driving force for Cl^- and fluid movements. We investigated whether a deficiency in K_Ca 3.1 (K_Ca 3.1^-/- ) protects against fatal pulmonary circulatory collapse in mice after pharmacological activation of the calcium-permeable TRP subfamily vanilloid type 4 (TRPV4) channels.

Experimental approach

An opener of TRPV4 channels, GSK1016790A, was infused in wild-type (wt) and K_Ca 3.1^-/- mice; haemodynamic parameters, histology

SUBMITTER: Wandall-Frostholm C 

PROVIDER: S-EPMC4562510 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature