Vascular remodelling in physiology and disease is substantially dependent on vascular smooth muscle cells and endothelial cells that switch to phenotypes characterised by increased proliferation, migration etc. We are seeking to understand ion channels of these processes, particularly with reference to diseased human tissues. Data are consistent with specific potassium channel types, Kca3.1 and Kv1.3, causing membrane hyperpolarisation that drives calcium entry through non-voltage-gated calcium channels. A mixture of calcium-selective and calcium-permeable non-selective cationic channels is involved. An apparently special player is the TRPC1 channel subunit, which is up-regulated in vascular injury and promotes hyperplasia of smooth muscle cells in human saphenous vein (Kumar et al 2006 Circ Res 98, 557-). TRPC1 forms heteromultimeric assemblies with other TRP channel subunits that include TRPC5 (Xu et al 2006 Circ Res 98, 1381-). Endogenous vascular TRPC1-TRPC5 channels are stimulated by a range of factors, but particularly important are likely to be specific oxidized phospholipids, acting through Gi/o-protein signalling without calcium-release (AL-Shawaf et al 2010, ATVB 30, 1453-). Such lipids are suggested to be pivotal players in innate immunity and atherosclerosis. Other types of calcium channel subunit and regulator also contribute in vascular remodelling: One of them is STIM1, which shows dominant plasma membrane localisation in vascular smooth muscle cells and co-localises with a pool of TRPC1 (Li et al 2008 Circ Res 103, e97-). STIM1 is a single-pass membrane protein with promiscuity in its function, in part because it also plays a role in calcium-release activated calcium (CRAC) channels, which are formed by Orai1 and underlie calcium entry evoked by the vascular smooth muscle cell recruiter, PDGF (Li et al BJP 164, 382-). The key stimulator of endothelial cells and angiogenesis, VEGF, also signals through such CRAC channels (Li et al 2011, Circ Res 108, 1190-). Potent small molecule inhibitors of these channels are starting to emerge and may provide valuable foundations for novel therapeutics (Li et al BJP 164, 382-). Our understanding of the molecular complexities of the different calcium channels and their inter-relationships is, however, in its infancy and should be further advanced.