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Aldosterone acts in the Nucleus Tractus Solitarius (NTS) to increase expression of vasopressin (AVP) in the Paraventricular Nucleus of the Hypothalamus (PVN)
Author(s) -
Cho Namjik,
Scheuer Deborah
Publication year - 2013
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.27.1_supplement.927.15
Subject(s) - medicine , endocrinology , rostral ventrolateral medulla , vasopressin , hypothalamus , aldosterone , solitary nucleus , angiotensin ii , amygdala , nucleus , renin–angiotensin system , solitary tract , chemistry , biology , medulla oblongata , receptor , blood pressure , central nervous system , neuroscience
Aldosterone (Aldo) is gaining attention as a stress hormone and causative factor in hypertension. We previously reported that implantation of pellets consisting of 1% Aldo to produce localized increases in Aldo within the NTS enhanced the arterial pressure response to a novel stressor in chronically stressed male Sprague‐Dawley rats. To elucidate mechanisms contributing to the enhanced stress responsiveness in these rats, quantitative real‐time PCR was performed on punches obtained from the NTS, PVN, rostral ventrolateral medulla (RVLM) and amygdala (Amyg) (Sham and 1% Aldo, n=6 each). Gene expression was analyzed statistically as ΔCt using 18S rRNA expression as the internal control. Relative fold changes in mRNA expression were normalized to Sham rats. Compared with Sham pellets, Aldo significantly (P≤0.05) increased expression for AVP in the PVN (3.8 fold) and the angiotensin type 1 receptor in the RVLM (2.8 fold), but did not affect the expression of these genes in the NTS. Aldo also significantly reduced expression of glial marker CD11b in the Amyg (0.6 fold) but not in the other regions tested. The results suggest that Aldo may act in the NTS to enhance stress responsiveness by increasing vasopressin synthesis and enhancing actions of angiotensin II in the RVLM. Supported by NIH #HL76807 and AHA 10GRNT4460047.