Nomenclature	VRAC
Activators	GTPγS
Endogenous channel blockers	intracellular Mg2+, arachidonic acid
Channel blockers	1,9‐dideoxyforskolin, 9‐anthroic acid, DCPIB, DIDS, IAA‐94, NPPB, NS3728, carbenoxolone, clomiphene, diBA‐(5)‐C4, gossypol, mefloquine, mibefradil, nafoxidine, nordihydroguiaretic acid, quinidine, quinine, tamoxifen
Functional Characteristics	γ = 10–20 pS (negative potentials), 50–90 pS (positive potentials); permeability sequence SCN > I > ${\text{NO}}_3^{-}$>Br‐> Cl‐> F‐> gluconate; outward rectification due to voltage dependence of γ; inactivates at positive potentials in many, but not all, cell types; time dependent inactivation at positive potentials; intracellular ionic strength modulates sensitivity to cell swelling and rate of channel activation; rate of swelling‐induced activation is modulated by intracellular ATP concentration; ATP dependence is independent of hydrolysis and modulated by rate of cell swelling; inhibited by increased intracellular free Mg2+ concentration; swelling induced activation of several intracellular signalling cascades may be permissive of, but not essential to, the activation of VRAC including: the Rho‐Rho kinase‐MLCK; Ras‐Raf‐MEK‐ERK; PIK3‐NOX‐H2O2 and Src‐PLCγ‐Ca2+ pathways; regulation by PKCα required for optimal activity; cholesterol depletion enhances activity; activated by direct stretch of β1‐integrin
Comments	VRAC is also activated by cell swelling and low intracellular ionic strength. VRAC is also blocked by chromones, extracellular nucleotides and nucleoside analogues