In urethane-anesthetized rats, in control conditions (after salin

In urethane-anesthetized rats, in control conditions (after saline injected into the commNTS), a brief period of hypoxia (8–10%

O2 in the breathing air for 60 s) produced an initial increase in MAP (26 ± 5 mmHg) in the first 5–10 s followed by a decrease in MAP (−47 ± 6 mmHg) that reach the maximum at the end of the period of hypoxia (Fig. 2A1 and B1). In these conditions, hypoxia also increased sSND (283 ± 19% of the baseline) and mvPND (calculated as the product of phrenic nerve frequency and amplitude – f × a – a measure of the total phrenic neural output) (149 ± 25% of the baseline) ( Fig. 2A1, C and D). Injection of muscimol (100 pmol/50 nl) into the commNTS did not change resting MAP (112 ± 3 mmHg, vs. saline: 110 ± 5 mmHg, p > 0.05), sSND and mvPND ( Fig. 2A2). The PND amplitude (98 ± 6% of control; p > 0.05) and duration (from 0.48 ± 0.02 to 0.47 ± 0.05 s, p > 0.05) also did not change. INCB024360 concentration Muscimol injected within the commNTS blocked the pressor response (5 ± 2 mmHg, p < 0.01) and reduced sympathoexcitation (93 ± 15% of the baseline, p < 0.01) and the increase in PND (20 ± 6% of the baseline, p < 0.01) produced by hypoxia ( Fig. 2A2, 2B–D). Muscimol into the

commNTS also increased the hypotension produced by 60 s of hypoxia in anesthetized rats (−63 ± 4 mmHg, p < 0.05) ( Fig. 2A2 and SB431542 datasheet B). In conscious rats, in control conditions (after saline injected into the commNTS), 60 s of hypoxia (8–10% O2 in the inspired

air) under normocapnia increased MAP (36 ± 3 mmHg), fR (60 ± 4 breaths/min), VT (4 ± 0.3 ml/kg) and V˙E (641 ± 28 ml/min/kg) and Dolutegravir cell line reduced HR (−96 ± 6 bpm) (Fig. 3A–E). Injection of muscimol (100 pmol/50 nl) into the commNTS, in conscious rats, did not change resting MAP (113 ± 6 mmHg, vs. saline: 117 ± 5 mmHg, p   > 0.05) and HR (335 ± 21 bpm, vs. saline: 341 ± 18 bpm, p   > 0.05). Muscimol injection within the commNTS reduced the increase on MAP (16 ± 2 mmHg, p   < 0.05), fR (26 ± 3 breaths/min, p   < 0.05), VT (1.8 ± 0.2 ml/kg, p   < 0.05) and V˙E (250 ± 17 ml/kg/min, p < 0.01) and blocked the bradycardia (1 ± 2 bpm, p < 0.01) produced by hypoxia ( Fig. 3A–F). In urethane-anesthetized rats, in control conditions (after saline injected into the commNTS), hypercapnia (from 5% to 10% CO2 for 5 min) produced an immediate hypotension (−22 ± 4 mmHg) that was gradually reduced with MAP returning to or slightly above control levels at the end of hypercapnia. Immediately after stopping hypercapnia (returning to 5% CO2), MAP increased (27 ± 5 mmHg) and returned to control values after around 5 min (Fig. 4A1 and B). In control condition, hypercapnia also increased sSND (108 ± 13% of baseline at 5% CO2) and mvPND (111 ± 8% of the baseline at 5% CO2) (Fig. 4A1, C and D).

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