Fig. 2.

Neuronal excitability to NE following myocardial infarction (MI) is altered by ANG II modulators. F-I curves were determined in animals 7 wk after surgical MI with and without NE application in animals with MI alone (n = 56 cells), or combined with 6 wk of treatment with captopril (n = 32 cells), losartan (n = 28 cells), or CGP42112A (n = 42 cells). NE increases neuronal firing over baseline in both control and MI preparations (A; *P < 0.05 vs. control at that stimulus intensity). In addition, in MI animals, the effect of NE was significantly greater than NE in control animals at the higher stimulus intensities (A; #P < 0.05 vs. control NE at that stimulus intensity). The same MI with NE data are shown in B–D for comparison. There were no changes in baseline excitability (in the absence of NE) with the different drug treatment (control with drug vs. MI with drug, B–D). Captopril-treated MI animals showed the same increase in excitability with NE as untreated MI with NE (B; *P < 0.05 vs. captopril control at that stimulus intensity). With losartan treatment, NE still increased excitability over baseline in MI animals treated with losartan (C; *P < 0.05 vs. losartan control at that stimulus intensity). There was no significant difference between untreated MI with NE and losartan-treated MI with NE at any stimulus intensity. MI animals treated with CGP42112A no longer showed a significant increase in excitability with NE vs. CGP42112A controls (D; *P < 0.05 vs. CGP 42112A control at that stimulus intensity). Significant differences were determined by Kruskal-Wallis ANOVA on ranks for each stimulus intensity with nonparametric post hoc comparisons.