Previously, we reported that global genetic deletion of 2 pore-domain TWIK-relative acid-sensitive potassium channels, TASK-1 and TASK-3, from mice produces striking aldosterone excess, low renin, and hypertension.
Potassium channel subfamily K member 3 (KCNK3) has been reported to play important roles in membrane potential conduction, pulmonary hypertension and thermogenesis regulation in mammals.
A trend toward positive association (P = .05) was also found between AP and a single nucleotide polymorphism in KCNK3, a gene known to be involved in increased susceptibility to hypertension.
In 2013, KCNK3 (TASK1), which encodes a type of two-pore domain potassium channel, was shown to be a predisposing gene for PAH by genetic mutation, and it was added to the PAH classification at the Fifth World Symposium on Pulmonary Hypertension (Nice International Conference).
Intergenic polymorphism rs10792367 between OAT1 and OAT3 is not associated with hypertension, but appears to be involved in between-individual variations in antihypertensive responses to HCTZ.