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Role of NTS P2x receptors in cardiovascular adjustments during alerting defense reactions
Author(s) -
Korim Willian Seiji,
FerreiraNeto Marcos L,
Cravo Sergio L.D.
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a878-a
The aim of this study was to verify the role of NTS P2x receptors in hemodynamic adjustments during electrical stimulation of the hypothalamic defense area (HDA) in anesthetized rats. Male Wistar rats were anesthetized, paralized and artificially ventilated. Mean arterial pressure (MAP), heart rate (HR) and hindquarter blood flow (HQBF) were recorded. Hindquarter vascular conductance (HQVC) was determined by the ratio MAP/HQBF. HDA stimulation (150 μA;0.6 ms;100 Hz;N=9) evoked hypertension (36±6 mmHg), tachycardia (58±13 bpm) and vasodilation (peak HQVC: 171±17%). After NTS bilateral blockade with the P2x antagonist suramin (100 pmol/50 nl) pressor and heart rate responses to HDA stimulation remained unchanged (32±5 mmHg; 31±6 bpm, respectively). Hindquarter vasodilation however was reduced in magnitude (57±16%) and duration. MAP, HR and HQVC were not affected by suramin microinjetction in the NTS. In the second group (N=8) microinjection of the P2x agonist α,β‐meATP (100 pmol/50 nl) in the NTS evoked hypotension (−46±4 mmHg), bradycardia (−66±17 bpm) and hindlimb vasodilation (peak: 62±8%). Blockade with suramin abolished the hypotension (−7±2 mmHg) and the vasodilation (11±2%) due to α,β‐meATP in the NTS but did not change the bradycardia (−40±17 bpm) nor the basal levels of MAP, HR and HQVC. Our results indicated that hindquarter vasodilation during defense reactions are mediated by P2x receptors in the NTS. Support by: CAPES, CNPq.