Table 3.
Effect of angiotensin-coverting enzyme and chymase inhibitors on mNTS neuronal activity
| Firing Rate (spikes/s) |
||||
|---|---|---|---|---|
| Drug | Route | Before | After | Increase |
| 1. PE (2–4 μg/kg) | Intravenous | 7.3 ± 0.8 | 18.1 ± 1.2 | 10.7 ± 0.8 |
| 2. l-Glu (5 mM) | Pressure ejection | 7.6 ± 0.9 | 20.8 ± 1.6 | 13.2 ± 1.4 |
| 3. aCSF | Pressure ejection | 7.1 ± 0.9 | 7.3 ± 0.8 | 0.2 ± 0.1 |
| 4. ANG-(1–12) (0.06 mM) | Pressure ejection | 7.3 ± 0.8 | 16.7 ± 1.7 | 9.5 ± 1.1† |
| 5. Captopril (50 mM) + chymostatin (0.5 mM) | Pressure ejection | 7.9 ± 0.8 | 7.3 ± 0.8 | 0.3 ± 0.2 |
| 6. ANG-(1–12) (0.06 mM) | Pressure ejection | 7.5 ± 0.8 | 8 ± 0.9 | 0.5 ± 0.1* |
Values are means ± SE; n = 23 barosensitive neurons in 12 rats. Drugs were injected or pressure ejected in the same sequence as indicated (1–6). The volume of pressure ejection of each drug was 2 nl. Intravenous phenylephrine (PE) and pressure ejections of l-glutamate (l-Glu) and ANG-(1–12) significantly increased neuronal firing (P < 0.001 each). The increase in firing induced by pressure ejection of ANG-(1–12) was significantly attenuated after pressure ejection of captopril and chymostatin compared with the increase in firing before the application of these inhibitors (
*
P < 0.001).
†
The onset time of these effects was 15.9 ± 1.7 s.