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A2 noradrenergic neurons inhibit osmoreceptor‐induced pressor responses.
Author(s) -
FreiriaOliveira Andre Henrique,
Blanch Graziela Torres,
Pedrino Gustavo R.,
Cravo Sergio L.,
Colombari Eduardo,
Menani Jose Vanderlei,
Colombari Debora S. A.
Publication year - 2008
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.22.1_supplement.738.3
Subject(s) - osmoreceptor , endocrinology , medicine , solitary tract , chemistry , mean arterial pressure , angiotensin ii , tonicity , blood pressure , heart rate , receptor
A previous study showed that intragastric (ig) 2 M NaCl load increases mean arterial pressure (MAP) in rats with chronic electrolytic lesions of the commissural nucleus of the solitary tract (commNTS), but not in sham rats, suggesting that commNTS mechanisms inhibit pressor responses to osmoreceptor activation. In the present study we investigated the effects of ig 2 M NaCl load on MAP and heart rate (HR) in rats with lesions of the A2 noradrenergic neurons located in the NTS. Male Wistar rats (280–320 g) were submitted to lesions of DβH‐containing neurons in the commNTS achieved by injections of anti‐DβH‐saporin (12.6 ng/60 nl, n=11). Sham rats received injections of immunoglobulin‐G‐saporin (12.6 ng/60 nl, n = 5). Thirty days after saporin injections, MAP and HR were recorded for 60 min before and 60 min after ig 2 M NaCl load (2 ml). Intragastric 2 M NaCl increased MAP in A2 lesioned rats (14 ± 2 mmHg), but not in sham rats (3 ± 2 mmHg), without changing HR in both groups. A2 lesions produced no change on baseline MAP (112 ± 2 vs. sham: 118 ± 4 mmHg) and HR (341 ± 12 vs. sham: 382 ± 26 bpm) and also on baro and chemoreflex tested previously to ig 2 M NaCl. The results show that lesions of A2 noradrenergic neurons in the NTS facilitate pressor responses produced by increases in plasma osmolality, suggesting that A2 neurons are part of the mechanisms that inhibits osmoreceptor‐induced pressor responses. Supported by CNPq, FAPESP.