The myogenic response allows arteries and arteriole to react to changes in blood pressure, thus keeping blood flow within the vessel constant. It has been known for many years that ion channels on smooth muscle cells respond to stretch. However, the identity of the stretch-sensitive channels that serve this function in the retina are not known. Some clues come from studies in cerebral vasculature, which highlight a role for transient receptor potential (TRP) channels. In this issue,
McGahon et al.1 show that transient receptor potential channels (Cannonical C1, Melastatin M7, Vallinoid V1, V2, and V4, as well as Polycystic P1) are expressed on rat retinal arterioles. The team patch clamped vascular smooth muscle cells embedded within retinal vessels but electrical uncoupled from their neighbors.
McGahon et al.1 show that the response to hypotonic stretch can be blunted by applying a range of pharmacological and antibody inhibitors of TRPV2 channels, whereas TRPC1, M7, V1, and V4 appear to play a negligible role in the myogenic response. Thus the myogenic response in retinal arterioles appears to be mediated by TRPV2 channels which is different to those mediating similar local responses in cerebral vessels. This study advances our understanding of the mechanisms controlling ocular blood flow autoregulation. Such insights critically inform our search for pathogenic and therapeutic pathways in a range of retinal conditions in which vascular dysregulation has been implicated.