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Na + ‐independent, nifedipine‐resistant rat afferent arteriolar Ca 2+ responses to noradrenaline: possible role of TRPC channels
Author(s) -
Salomonsson M.,
Braunstein T. H.,
HolsteinRathlou N.H.,
Jensen L. J.
Publication year - 2010
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2010.02141.x
Subject(s) - trpc , nifedipine , transient receptor potential channel , trpc5 , chemistry , medicine , endocrinology , depolarization , channel blocker , amiloride , biophysics , receptor , biology , calcium , sodium , biochemistry , organic chemistry
Aim: In rat afferent arterioles we investigated the role of Na + entry in noradrenaline (NA)‐induced depolarization and voltage‐dependent Ca 2+ entry together with the importance of the transient receptor potential channel (TRPC) subfamily for non‐voltage‐dependent Ca 2+ entry. Methods: R340/380 Fura‐2 fluorescence was used as an index for intracellular free Ca 2+ concentration ([Ca 2+ ] i ). Immunofluorescence detected the expression of TRPC channels. Results: 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 R 340/380 (control response 123%). However, as the R 340/380 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 + /Ca 2+ 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 μ m ) and Gd 3+ (100 μ m ) further reduced the plateau Ca 2+ responses to NA (from 117% to 102% and from 117% to 110% respectively). Conclusion: We found that Na + is not crucial for the NA‐induced depolarization that mediates Ca 2+ entry via L‐type channels. In addition, the results are consistent with the idea that TRPC1/3/6 Ca 2+ ‐permeable cation channels expressed in afferent arteriolar smooth muscle cells mediate Ca 2+ entry during NA stimulation.