Na+-independent, nifedipine-resistant rat afferent arteriolar Ca2+ responses to noradrenaline: possible role of TRPC channels

作者：Salomonsson M^*; Braunstein T H; Holstein Rathlou N H; Jensen L J

来源：Acta Physiologica, 2010, 200(3): 265-278.

DOI：10.1111/j.1748-1716.2010.02141.x

• adrenoceptors
• afferent arteriole
• renal haemodynamics
• ROC
• VSMC

Aim:
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.
Methods:
R-340/380 Fura-2 fluorescence was used as an index for intracellular free Ca2+ concentration ([Ca2+](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+/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 mu m) and Gd3+ (100 mu m) further reduced the plateau Ca2+ 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 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.

• 出版日期2010-11