GABA and nitric oxide in the PVN are involved in arterial pressure control but not in the chemoreflex responses in rats

GABAergic, nitrergic and glutamatergic mechanisms in the PVN on the baseline mean arterial pressure (MAP), heart rate (HR) and on the cardiovascular responses to chemoreflex activation in awake rat were evaluated. Chemoreflex was activated with KCN before and after microinjections into the PVN. Bicuculline into the PVN increased baseline MAP (94 ± 3 vs 113 ± 5 mmHg) and HR (350 ± 9 vs 439 ± 18 bpm) but had no effect on the pressor (49 ± 5 vs 47 ± 6 mmHg) or bradicardic (− 213 ± 23 vs − 256 ± 42 bpm) responses (n = 7). Kynurenic acid into the PVN (n = 6) produced no significant changes in the MAP (98 ± 3 vs 100 ± 3 mmHg), HR (330 ± 5 vs 339 ± 12 mmHg) or in the pressor (50 ± 4 vs 42 ± 4 mmHg) and bradicardic (− 252 ± 4 vs − 285 ± 16 bpm) responses to chemoreflex. L-NAME into the PVN (n = 8) produced increase in the MAP (94 ± 3 vs 113 ± 5 mmHg) and HR (350 ± 9 vs 439 ± 18 bpm) but had no effect on the pressor (52 ± 5 vs 47 ± 6 mmHg) or bradicardic (− 253 ± 19 vs − 320 ± 25 bpm) responses to chemoreflex. We conclude that GABAA and nitric oxide in the PVN are involved in the maintenance of the baseline MAP but not in the modulation of the responses to chemoreflex. The results also show that Glutamate receptors in the PVN are not involved in maintenance of the baseline MAP, HR or in the cardiovascular responses to chemoreflex in awake rats.