Aldosterone infusion into the 4th ventricle produces sodium appetite with baroreflex attenuation independent of renal or blood pressure changes

S Gasparini; M.R Melo; G.M.F Andrade-Franzé; J.C Geerling; J.V Menani; E Colombari

doi:10.1016/j.brainres.2018.06.023

Back

Aldosterone infusion into the 4th ventricle produces sodium appetite with baroreflex attenuation independent of renal or blood pressure changes

Journal article

Open access

Peer reviewed

Aldosterone infusion into the 4th ventricle produces sodium appetite with baroreflex attenuation independent of renal or blood pressure changes

S Gasparini, M.R Melo, G.M.F Andrade-Franzé, J.C Geerling, J.V Menani and E Colombari

Brain research, Vol.1698, pp.70-80

11/01/2018

DOI: 10.1016/j.brainres.2018.06.023

PMID: 29928872

Files and links (1)

url

https://doi.org/10.1016/j.brainres.2018.06.023View

Published (Version of record) Open Access

Abstract

•Aldosterone into the 4th V activates HSD2 neurons in the NTS to cause sodium intake.•Aldosterone into the 4th V and sodium intake reduces baroreflex sensitivity.•Aldosterone into the 4th V produces no change in blood pressure and renal excretion. Aldosterone infusion into the 4th ventricle (4th V), upstream the nucleus of the solitary tract (NTS), produces strong 0.3 M NaCl intake. In the present study, we investigated whether aldosterone infusion into the 4th V activates HSD2 neurons, changes renal excretion, or alters blood pressure and cardiovascular reflexes. Chronic infusion of aldosterone (100 ng/h) into the 4th V increased daily 0.3 M NaCl intake (up to 44 ± 10, vs. vehicle: 5.6 ± 3.4 ml/24 h) and also c-Fos expression in HSD2 neurons in the NTS and in non-HSD2 neurons in the NTS. Natriuresis, diuresis and positive sodium balance were present in rats that ingested 0.3 M NaCl, however, renal excretion was not modified by 4th V aldosterone in rats that had no access to NaCl. 4th V aldosterone also reduced baroreflex sensitivity (−2.8 ± 0.5, vs. vehicle: −5.1 ± 0.9 bpm/mmHg) in animals that had sodium available, without changing blood pressure. The results suggest that sodium intake induced by aldosterone infused into the 4th V is associated with activation of NTS neurons, among them the HSD2 neurons. Aldosterone infused into the 4th V in association with sodium intake also impairs baroreflex sensitivity, without changing arterial pressure.

Sodium excretion

Sodium ingestion

Aldosterone

HDS2 neurons

Baroreflex

Details

Title: Subtitle: Aldosterone infusion into the 4th ventricle produces sodium appetite with baroreflex attenuation independent of renal or blood pressure changes
Creators: S Gasparini - Department of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara, SP, Brazil
M.R Melo - Department of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara, SP, Brazil
G.M.F Andrade-Franzé - Department of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara, SP, Brazil
J.C Geerling - Departament of Neurology, University of Iowa Carver College of Medicine, Iowa City, IA, USA
J.V Menani - Department of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara, SP, Brazil
E Colombari - Department of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara, SP, Brazil
Resource Type: Journal article
Publication Details: Brain research, Vol.1698, pp.70-80
Publisher: Elsevier B.V
DOI: 10.1016/j.brainres.2018.06.023
PMID: 29928872
ISSN: 0006-8993
eISSN: 1872-6240
Language: English
Date published: 11/01/2018
Academic Unit: Neurology; Iowa Neuroscience Institute
Record Identifier: 9984020651102771

Metrics

19 Record Views

10 Times Cited - Web of Science