Lesion of the commissural nucleus of the solitary tract/A2 noradrenergic neurons facilitates the activation of angiotensinergic mechanisms in response to hemorrhage

- Lesions of the cNTS/A2 neurons facilitate the recovery of hemorrhage-induced hypotension.
- Lesions of the cNTS/A2 seem to increase central and peripheral angiotensinergic mechanisms.
- cNTS/A2 neurons are not involved with baroreflex and chemoreflex responses.
- cNTS/A2-lesions do not promote arterial pressure lability.

In the present study, we investigated the effects of lesions of A2 neurons of the commissural nucleus of the solitary tract (cNTS) alone or combined with the blockade of angiotensinergic mechanisms on the recovery of arterial pressure (AP) to hemorrhage in conscious rats. Male Holtzman rats (280-320 g) received an injection of anti-dopamine-beta-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2-lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl, sham, n = 24) into the cNTS and 15-21 days later had a stainless steel cannula implanted in the lateral ventricle. After 6 days, rats were submitted to hemorrhage (four blood withdrawals, 2 ml/300 g of body weight every 10 min). Both cNTS/A2-lesioned and sham rats had similar hypotension to hemorrhage (−62 ± 7 and −73 ± 7 mmHg, respectively), however cNTS/A2-lesioned rats rapidly recovered from hypotension (−5 ± 3 mmHg at 30 min), whereas sham rats did not completely recover until the end of the recording (−20 ± 3 mmHg at 60 min). Losartan (angiotensin type 1 receptor antagonist) injected intracerebroventricularly (100 μg/1 μl) or intravenously (i.v.) (10 mg/kg of body weight) impaired the recovery of AP in cNTS/A2-lesioned rats (−24 ± 6 and −35 ± 7 mmHg at 30 min, respectively). In sham rats, only i.v. losartan affected the recovery of AP (−39 ± 6 mmHg at 60 min). The results suggest that lesion of the A2 neurons in the cNTS facilitates the activation of the angiotensinergic pressor mechanisms in response to hemorrhage.