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. 2012 Oct;343(1):97–105. doi: 10.1124/jpet.112.196626

Fig. 1.

Fig. 1.

Release of NE from cardiac synaptosomes during 30-min hypoxia. Bars (means ± S.E.M.) represent the hypoxia-induced increase in NE release above the normoxic basal level of 273 ± 11.5 pmol/mg protein (n = 49). A, activation of ALDH2 with Alda-1 (20 μM; 12 min) reduces hypoxia-induced NE release. Desensitization of ALDH2 with GTN (2 μM; 30 min) prevents the effect of Alda-1 (n = 7–12). *, P < 0.05 versus hypoxia. #, P < 0.05 versus Alda-1 by unpaired t test. B, PKCε activation with ΨεRACK (PKCε activator; 500 nM; 12 min) reduces hypoxia-induced NE release. ALDH2 desensitization with GTN (2 μM; 30 min) prevents the effect of ΨεRACK (n = 7–8). *, P < 0.05 versus hypoxia. #, P < 0.05 versus ΨεRACK by unpaired t test. C, activation of adenosine A1 receptor with 2′-MeCCPA (A1R agonist; 10 nM; 12 min) diminishes hypoxia-induced NE release. ALDH2 desensitization with GTN (2 μM; 30 min) and PKCε blockade with εV1–2 (PKCε inhibitor; 1 μM; 20 min) each prevents the effect of 2′-MeCCPA (n = 7–10). **, P < 0.005 versus hypoxia. #, P < 0.05 versus 2′-MeCCPA by unpaired t test. D, blockade of adenosine A1-receptor with DPCPX (A1R antagonist; 300 nM; 12 min) enhances hypoxia-induced NE release (n = 15–17). *, P < 0.05 versus hypoxia by unpaired t test. E, selective activation of adenosine A3 receptor with IB-MECA (A3R agonist; 50 nM; 12 min) reduces hypoxia-induced NE release. ALDH2 desensitization with GTN (2 μM; 30 min) and PKCε blockade with εV1–2 (1 μM; 20 min) each prevents the effect of IB-MECA (n = 7–11). **, P < 0.01 versus hypoxia. ##, P < 0.005 versus IB-MECA. ###, P < 0.001 versus IB-MECA by unpaired t test. F, blockade of adenosine A3 receptor with MRS1523 (A3R antagonist; 100 nM; 12 min) enhances hypoxia-induced NE (n = 7–9). *, P < 0.05 versus hypoxia by unpaired t test.