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. Author manuscript; available in PMC: 2011 Mar 5.
Published in final edited form as: Circ Res. 2009 Dec 31;106(4):739–747. doi: 10.1161/CIRCRESAHA.109.206763

Figure 6.

Figure 6

Pharmacological depletion of intracellular Ca2+ stores restores nifedipine (Nif) sensitivity to depolarization-induced contractions in rat MV. Blocking store-operated Ca2+ release with Gd3+ (A, 100 µmol/L) or La3+ (B, 100 µmol/L) did not reduce venous KCl-induced constriction or restore sensitivity to Nif in veins. (n = 4–5) (C) KCl-induced constrictions after Thaps were blocked 80% by Nif (10 µmol/L). (n = 6) (D) Store depletion by caffeine (Caf, 10 mmol/L) also resulted in sensitivity to block by Nif. (E) Using ryanodine (Ryan, 10 nmol/L) to deplete intracellular Ca2+ stores also resulted in MV sensitivity to nifedipine, (n = 5–6), as did incubating with 2-APB (100 µmol/L) (F) (n = 6). * = significant difference from Control (Con), p<0.05; † = significant difference between Thaps, Caf, Ryan, or 2-APB in the presence and absence of Nif.