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. 2013 Aug 2;305(7):H980–H986. doi: 10.1152/ajpheart.00255.2013

Fig. 3.

Fig. 3.

Neuronal NE reuptake transporter (NET) inhibitor desipramine (DMI; 1 μM) significantly (*P < 0.05) increased [3H]NE release in response to electrical field stimulation (S1 vs. S2, 5 Hz) of isolated atria in the WKY (n = 8, raw data in A; P < 0.01, ANOVA) and SHR (n = 10, raw data in B; P < 0.01, ANOVA). However, after desipramine pretreatment the difference in [3H]NE release between the SHR and WKY was abolished (group mean data in E, unpaired t-test). The α2-receptor antagonist yohimbine (1 μM) had no effect on [3H]NE release in the WKY (n = 8, raw data trace in C) but significantly increased the release of [3H]NE in the SHR (n = 7, raw data trace in D; P < 0.001, ANOVA), The difference in [3H]NE release in response to field stimulation between the SHR and WKY increased significantly in the presence of yohimbine (**P < 0.01, unpaired t-test, group mean data in E).