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Glucocorticoids Enhance Expression of Angiotensin II Type 1 Receptors in the Dorsal Hindbrain
Author(s) -
Su Ye,
Daubert Daisy L.,
Sumners Colin,
Speth Robert,
Li Hongwei,
Scheuer Deborah 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.1171.6
Subject(s) - medicine , endocrinology , corticosterone , solitary tract , angiotensin ii , receptor , chemistry , hindbrain , phenylephrine , biology , central nervous system , blood pressure , hormone
We have shown that increases in dorsal hindbrain (DHB) corticosterone (Cort) enhance the blood pressure response to acute stress. Stress activates brain angiotensin type I receptors (AT1R), and glucocorticoids can increase AT1R expression. Thus, we hypothesized that chronic increases in DHB Cort elevate AT1R expression and binding within the nucleus of solitary tract (NTS). Male Sprague‐Dawley rats were treated with sham, 50% or 100% Cort DHB pellets, or 100% Cort pellets subcutaneously (sc) for 6 days. AT1R mRNA was analyzed by quantitative real‐time PCR, and the binding of AT1R was assessed by autoradiography and quantitative densitometry in the NTS and the rostral ventral lateral medulla (RVLM). Data were analyzed by ANOVA. In the caudal NTS, AT1R binding density was significantly increased (P<0.05) in 50% and 100% DHB Cort‐treated rats (1527±54 and 1436±42 fmol/g) relative to DHB sham‐treated rats (1215±57 fmol/g). However, in the rostral NTS and RVLM, there were no effects of DHB Cort treatment on AT1R binding. AT1R mRNA in the NTS was significantly (P<0.05) increased in DHB 50% Cort‐treated rats relative to DHB Sham‐ and sc‐treated rats (1.77±0.13 versus 0.73±0.1 and 0.97±0.1 arbitrary units). The increase in mRNA in 100% DHB Cort‐treated rats was not significant. We conclude that chronic elevations in DHB Cort increase AT1R mRNA and binding within the NTS. Funded by NIH grant number HL 076807.