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In rat afferent arterioles we investigated the role of Na+ entry in noradrenaline (NA)-induced depolarization and voltage-dependent Ca2+ entry together with the importance of the transient receptor potential channel (TRPC) subfamily for non-voltage-dependent Ca2+ entry.R340/380 Fura-2 fluorescence was used as an index for intracellular free Ca2+ concentration ([Ca2+]i). Immunofluorescence detected the expression of TRPC channels.TRPC 1, 3 and 6 were expressed in afferent arteriolar vascular smooth muscle cells. Under extracellular Na+-free (0 Na) conditions, the plateau response to NA was 115% of the baseline R340/380 (control response 123%). However, as the R340/380 baseline increased (7%) after 0 Na the plateau reached the same level as during control conditions. Similar responses were obtained after blockade of the Na+/Ca2+ exchanger. The L-type blocker nifedipine reduced the plateau response to NA both under control (from 134% to 116% of baseline) and 0 Na conditions (from 112% to 103% of baseline). In the presence of nifedipine, the putative TRPC channel blockers SKF 96365 (30 μm) and Gd3+ (100 μm) further reduced the plateau Ca2+ responses to NA (from 117% to 102% and from 117% to 110% respectively).We found that Na+ is not crucial for the NA-induced depolarization that mediates Ca2+ entry via L-type channels. In addition, the results are consistent with the idea that TRPC1/3/6 Ca2+-permeable cation channels expressed in afferent arteriolar smooth muscle cells mediate Ca2+ entry during NA stimulation.