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Expression of Mineralocorticoid Receptors (MR) and Epithelial Na+ Channel (ENaC) Subunits in the Heart and Brain Nuclei of Rats Post‐MI
Author(s) -
ElAlfy Ahmed,
Wang HongWei,
Tan Junhui,
Speth Robert,
Leenen Frans HH
Publication year - 2007
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.21.6.a1270
Subject(s) - epithelial sodium channel , endocrinology , medicine , aldosterone , mineralocorticoid receptor , downregulation and upregulation , messenger rna , receptor , mineralocorticoid , in situ hybridization , chemistry , gene , sodium , organic chemistry , biochemistry
Blockade of central and peripheral MR in rats post MI attenuates sympathetic hyperactivity and ameliorates LV remodeling. The mechanisms involved are not yet clear. We studied mRNA expression of MR and ENaC (α, β, γ) subunits by real‐time qRT‐PCR and aldosterone binding densities by autoradiography in heart and brain nuclei of male Wistar rats at 2 & 4 wks post MI. Binding densities increased in LV and 2 brain nuclei, but decreased markedly in the infarct scar (table). MR mRNA decreased only at 2 wks; in SFO and OVLT (5.6±0.7 vs. 7.9±0.5, p<0.05; 2.9±0.4 vs. 5.4±0.6, p=0.05; MR/PGK [×10 −2 ]) and showed no changes in LV and other nuclei. ENaC mRNA levels significantly increased in the scar vs. non‐infarct LV & sham (41.0±6.0 vs. 3.8±1.0 & 1.5±0.4, for α; 11.3±1.0 vs. 0.3±0.1& non detectable levels for β, and 25.6±5.0 vs. 0.2±0.04 & 0.3±0.1for γ; ENaC/PGK [×10 −4 ]). These results indicate that in rats post MI, MR expression is differentially regulated in brain nuclei. Upregulation of aldosterone binding densities and ENaC transcription in heart and brain may contribute to LV remodeling.