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TRP channels provide the depolarisation initiating vasomotion and vessel tone in cerebral resistance arteries

Coordinated oscillations in diameter occur spontaneously in cerebral vessels and depend on the opening of voltage dependent calcium channels. We investigated the mechanism that provides the initial depolarisation required for vasomotion. Branches of juvenile rat basilar arteries were studied by measurement of diameter, calcium and membrane potential. Removal of extracellular calcium ([Ca2+]o) abolished vasomotion, relaxed arteries (125% resting vessel diameter, RVD), reduced intracellular Ca2+ ([Ca2+]I; 71%), but paradoxically depolarized cells (‐40mV to ‐27mV). Reduction of [Na+]o, from 140mM to 100mM, produced comparable effects, except that vessels hyperpolarized (‐52mV), even in the absence of [Ca2+]o. TRP channel blockers, SKF96365 and gadolinium, also relaxed vessels (111% RVD), abolished vasomotion, decreased [Ca2+]i (87%) and hyperpolarized (‐57mV) vessels. Depolarisation of SKF96365‐treated vessels with 40mM KCl reinstated vasomotion. Quantitative PCR revealed TRPC1 to be the predominantly expressed TRPC subtype and incubation with a function blocking TRPC1 antibody delayed the onset of vasomotion. We conclude that TRPC1 channels provide the initial depolarising current that activates voltage dependent calcium channels to provide vessel tone and initiate vasomotion. Selective TRP channel inhibition could provide a novel target for the treatment of cerebral vasospasm.