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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats

Full text
Author(s):
Ribeiro, Natalia [1] ; Martins Sa, Renato W. [1] ; Antunes, Vagner R. [1]
Total Authors: 3
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Av Prof Lineu Prestes 1524, BR-05508900 Sao Paulo, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Brain Research; v. 1748, DEC 1 2020.
Web of Science Citations: 0
Abstract

High salt intake is able to evoke neuroendocrine and autonomic responses that include vasopressin release and sympathoexcitation resulting in increasing in the arterial blood pressure (BP). The C1 neurons are a specific population of catecholaminergic neurons located in the RVLM region and they control BP under homeostatic imbalance. Thus, here we hypothesized that the ablation of C1 neurons mitigate the high blood pressure induced by high-salt intake. To test this hypothesis, we injected anti-D beta H-SAP saporin at the RVLM and monitored the BP in unanesthetized animals exposed to high salt intake of 2% NaCl solution for 7 days. The injection of anti-D beta H-SAP into the RVLM depleted 80% of tyrosine hydroxylase-positive neurons (TH+ neurons) in the C1, 38% in the A5, and no significant reduction in the A1 region, when compared to control group (saline as vehicle). High salt intake elicited a significant increase in BP in the control group, while in the anti-D beta H-SAP group the depletion of TH+ neurons prevents the salt-induced hypertension. Moreover, the low frequency component of systolic BP and pulse interval were increased by high-salt intake in control animals but not in anti-D beta H-SAP group, which indirectly suggests that the increase in the BP is mediated by increase in sympathetic activity. In conclusion, our data show that hypertension induced by high-salt intake is dependent on C1 neurons. (AU)

FAPESP's process: 16/21991-3 - Salt-induced hypertension: role of purinergic signaling in the neuronal cells at the hypothalamus level, and its correlation with the autonomic nervous system and blood pressure control
Grantee:Vagner Roberto Antunes
Support Opportunities: Regular Research Grants
FAPESP's process: 13/06206-0 - Gene expression changes of neuropeptides and proinflammatory factors of the hypothalamus and brainstem nucleus involved with cardiovascular regulation in diet-induced obesity animals
Grantee:Vagner Roberto Antunes
Support Opportunities: Regular Research Grants