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Time‐course changes on GABAergic and GLUergic gene expression in central autonomic areas: Effects of hypertension and aerobic training (T)
Author(s) -
Ruggeri Adriana,
Zampieri Thais T.,
Silva Sebastiao D.,
Ceroni Alexandre,
Michelini Lisete C.
Publication year - 2011
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.25.1_supplement.1054.2
Subject(s) - endocrinology , medicine , brainstem , gabaergic , bradycardia , heart rate , blood pressure , gene expression , chemistry , receptor , gene , biochemistry
T causes plastic & functional changes in autonomic pathways controlling cardiovascular function (Exp Physiol 2009;94:947). We sought now to identify and compare in normotensive and hypertensive rats the sequential effect of T on GABAergic and GLUergic neurons within central autonomic areas. WKY and SHR were trained (55% VO2 max, 5‐times/week, 1h/day) or kept sedentary (S) for 12 weeks. Pressure (AP), heart rate (HR) and mRNA expression were determined at weeks 0, 1, 2, 4, 8 and 12. After AP & HR measurement at rest, rats were anesthetized and perfused transcardiacally (PBS). Brains were removed, frozen and sliced to isolate ventral brainstem (VBS, comprising the RVLM) and hypothalamic (directed to PVN) areas; tissue samples were processed for Real Time PCR, with HPRT as the reporter gene. T‐induced resting bradycardia (~10% in both groups) appeared earlier in SHR (T2 vs T8 in WKY) while AP fall (−7% in SHR) was evident at T8‐T12. In the PVN of both groups GAD65/VGlut2 mRNA ratio was 5‐ to 6‐fold at S0 and increased even more during T (9‐ to 10‐fold at T1–T8). Compared to PVN, GAD expression was lower in the VBS (−44% and −29% in WKY and SHR) but was also increased by T (~55% at T2 in SHR and T8 in WKY). Similar time‐course changes of HR & AP and increased VBS & PVN GAD expression during T suggest that improvement of GABAergic signaling in these areas drives T‐induced autonomic control. Support CNPq, FAPESP

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